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1. preparation for patient in theater

Paperwork preparation;
 theatre list(-pts names,hospital number,pts location,operation details,operative surgeon )
 medical file available up to date (history and detail of daily physical examinations)
 Obtain consent
Patient preparation;
Lab preparation
I. FHG
II. GxM
III. U\E\C
IV. Urinalysis
V. Blood sugar
VI. Coagulation profile
Other preparation
 Urine catheter
 IV line and IV fluids
 NG tubes if necessary
 Antibiotic prophylactic (eg ceftiaxone 30 min before surgery)
 Mark the site
 Bowel preparations(types: stimulatant mechanical bowel preparation,osmotic mechanical bowel
preparation,stimulant left colon preparation,mechanical bowel preparation)
 Premedication:Anasthetic preparations(agent
used:diazepam,buscopan,pethidine)ranitidine(reduce gastric fluid pH and
volume.metoclopropamide(Plasil antiemetic.)atropine (reduce secretion)
Reasons for preparation of pts for theater
 To use safe anasthesia
 To help pts understand the procedure and get concent
 To discourage intra op,post op complications

2. Management of hemorrhagic shock

 Primary control bleeding source
 O-oxygenate pts
 R-restore circulation volume(secure large IV line, give IV fluids crystalloids:colloids:and blood
products
 D-drug therapy(inotropic agents:dopamine,vasopressor agents:norepinephrine,epinephrine
 E-evaluation response to therapy(vital signs,bp,urine input and output,capillary refill,CVP
monitor,blood analysis,and mental status
 R-remedy of underlying cause(eg shock,retroperitoneal hemorrhage,RX: immediate
exploration,isolation and ligation of bleeding vessels)

3.Causes of heart failure in young patient

 Myocarditis,viral,Bacterial
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 Rheumatic fever
 Endocarditis
 Congenital heart defects(,VSD,coartation of aorta,)
 Cardiomyopathy, (hypertrophic,dilated,restrictive)
 Tachyarrhythmias,supraventrivular tachycardia
 RHD
 Acute HTN
 High output severe anemia,thyrotoxicosis,arterovenous malformation
4.Types of catheter
Urine catheter
 foley catheter,(2 way foley,3 way foley catheter)
 intermittent or internal,
 condom or external catheter,
 robinson or flexible catherter,
 coude tipped catheter)
IV catheters
a) Peripheral iv catheter(arm and legs) periods 72-96h
b) Midline peripheral iv catheter(arm to axillary region(armpit)2-4weeks
c) Central venous catheters(from chest pushed to superior vena cava.)
Types:
 PICC
 Tunneled catheter(hickman)
 Implanted port(single port,double port)
 Non tunneled catheter(Quinton catheter,double or quadriple lumen
Sites:
 Subclavian,
 femoral,
 internal jugular

5.Causes of urethral strictures

Congenital
 Epispadis-urethral opening on dorsal aspect of penis
 Hypospadis-urethral opening at the ventral aspect of penis
 Urethral valve
 Congenital stenosis
Acquired
 traumatic( pelvic fracture, saddle injury, penile fracture),
 iatrogenic ( surgery ie prostatectomy, instrumentation ie indwelling catheter, urethral endoscopy),
 infectious (post gonorrhoea, TB urethritis, chlamidia, schistosomiasis)
6.Group of HIV drugs
Necleoside and Non nucleoside Protase inhibitor Entry inhibitors Intergrase strand
Necleotide reverse trasferase

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reverse transcriptase inhibitor

transcriptase inhibitors(NNRTI
inhibitors(NRTIs) s)
&(NtRTIs)
1. Lamivudine, 1. Nevirapine, 1) Lopinavir, 1. Fusion 1) Raltegravir)
2. Stavudine, 2. Efavirevz, 2) Ritonavir, inhibitors
3. Zidovudine, 3) Kaletra, (fuzeon),
4. Didanosine, 4) Atazanavir, 2. CCR5
5. Emtricitabine, 5) Indinavir, (maraviroc),
6. Abacavir, 6) Saquinavir
7. Tenofovir,

Indications to start HAART

i. HIV with TB
ii. HIV with HEPATITIS B
iii. CD4<350 regardless of the stage even if asymptomatic
iv. Stage 3 or 4 regardless of CD4 count
v. All children less than 18 month

7.Component of APGAR SCORE

SCORE 0 SCORE 1 SCORE 2
Appearance\color Blue\pale all over Blue Pink body Apperance
complexion extremity\pale
body
Pulse rate absent <100 bpm >100 bpm Pulse
Reflex irritability No response Grimace\Feeble Cry or pull away Grimace
cry-weak when stimulated
Activity (muscle none Some flexion normal muscle Activity
tone&movement some/floppy tone tone
Respiratory absent Weak Regular breathing Respiration
effort\breathing ,irregular,grasping
<3 critical. 4-7 fairly low. > 7 normal.

8.Reasons for isolation of patient

 Child with congenital immunodeficiency syndrome
 Psychiatric patient.on violent or suicidal thought
 Protect infection spread by hand,contact,with nonsterile equipment,feces,blood,blood
fluid,bedpan\urine
 Protect infection spread by respiratory droplet eg chicken pox,measle,mumps,TB
 Protect pts who are highly susceptible to infection eg pt with neuropenia,on anti ca
drugs,chemotherapy,severe immunocompromised pts.and Bone marrow transplant patient
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 Protect spread of highly contagious infection eg Ebola,anthrax ,haemorrhagic fever

9. What to check for in chest tube drainage

 Volume of drainage
 Colour
 Consistency
 Bubbling
 Movement with respiration

10. Indication for CS (cesarean section)

MATERNAL INDICATIONS-
1) previous uterine scar,
2) severe preeclampsia or eclampsia with unfavorable cervix,
3) Antepatum haemorrhage or placenta praevia,
4) Contracted pelvis,
5) Following repair of obstetric fistula vvf rvf,
6) Medical illness,
7) Prolonged labour,
8) Pelvic tumours obstructing labour,
9) Invasive carcinoma of the cervix,
10) infections hiv hsv hpv hbv.

FOETAL INDICATIONS-
1. Foetal distress,
2. Malpresentation and malposition,
3. Cord presentation or cord prolapse,
4. Multiple pregnancy ; first non cephalic, retained second twin, extreme prematurity, discordant foetal
growth, single amniotic sac, conjoined twins, > 2 twins.
5. Foetal anomalies ; hydrocephalus, sacral tumour, conjoined twins.
6. Foetal macrosomia weight > 4000g.
7. Others ; intrauterine growth retadation, oligohydramnios.

FETO-MATERNAL INDICATIONS-
1. failure to progress in labour,
2. Perimortem cs.
3. Lack of competency by service provider.
4 CPD)

11. Danger of meconium (rem - meconium aspiration syndrome)

 F- Fetal death
 I- Infection
 R- Respiratory distress syndrome at birth
 M- Meiconium aspiration syndrome
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 I- Intrauterine growth restriction

12. Stages of meconium stained liquor

3 stages :
1. yellow (transparent)
2. yellowish greenish(translucent)
3. Green(opaque)
CS from stage 2

13. Pulse rate in snake bite ( rapid pulse)

poisonous snakes of Kenya:
 Gaboon viper,
 Carpet viper,
 Puffadder,
 Egyptian cobra,
 Forest cobra,
 Black necked cobra,
 Black mamba,
 Green mamba,
 Jamesons mamba
signs of envoenvenomation:
vipers and adders:
 0-30min; severe radiating pain, local oedema.
 30min-1 hour; persistant pain, spreading oedema.
 1 hour+ ; Gi disorders, necrosis, infection, gangrene, haemorrhage, DIC.
Cobras and mambas:
 0-30min; moderate diffuse pain, numbness.
 30min-1 hour; intense asthenia, palpebral ptosis, neuro-muscular disorders.
 1 hour+; paralysis, asphyxia, collapse.
Mx:
FIELD:
I. move to safe place
II. Elevate the limb
III. remove constrictive clothes
IV. immobilize limb(splint,band)
V. no tourniquet
VI. nill per oral
HOSPITAL:
A. Primary survey ABC.Resuscitate if necessary
B. Secondary survey
 obtain iv line give fluids
 monitor vital signs
 clean bitten area,irrigate with nacl
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 elevate the limb

 give analgesia
 give tetanus toxoids
 Prophylactic antibiotics
 monitor for continuos swelling
 fasciotomy if indicated
 give antivenom if available & monitor allergic reaction
 Administration of FAV-Afrique; administer 20ml (2 ampules) of Fav-afrique as a direct IV injection
for 5 minutes or as a dilute infusion in 250ml of infusion fluid (0.9% Nacl or 5% glucose solution)
for 1 hour.
Types of snake venoms;
 Hemolytic,
 Cytolytic
 Neurotoxic.

14. Examination of ascites

A. Inspection:
 Abdominal distention
 Flank fullness
 Prominent abdominal veins
 Inverted umbilical
 Scarring for surgical marks
B. Palpation:
 fluid thrill,
C. percussion
 shifting dullness,
GRADES FOR ASCITES
 Grade 1:mild only visible on u\s and CT
 Grade 2:flank fullness & shifting dullness
 Grade 3:directly visible confirmed with fluid wave (thrill test)
Investigations
 paracentesis gross appearance
 protein level
 Albumin with SAAG
 cell count, culture
 Cytopathology
 SAAG
Classification: non peritoneal(transudate)&peritoneal(exudative)
Causes
HIGH SAAG(transudative) LOW SAAG(exudative)
Cirrhosis Cancer
HF Infection :TB,SBP
Hepatic venous occlusion e.g budd chiary Pancreatitis
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syndrome
Constrictive pericarditis Serositis
Kwashiorkor(childhood) Nephrotic syndrome
Portal vein thrombosis Hereditary angioedema

Complication of Ascites
 Spontaneous bacterial peritonitis(SBP)
 Hepatorenal syndrome
 Thrombosis of portal vein and splenic vein
 Weight loss or protein malnutrition
 Hepatic encephalopathy
DDX:
 Acute liver failure
 Hepatitis
 Liver cirrhosis
 Hepaterenal syndrome
 Budd chiary syndrome
 Nephrotic syndrome
 Cardiomegaly
 Portal HTN
Indication of tapping
 Dx new onset of ascites
 Ddx btw transudate and exudate ascites
 Detect present of cancerous cells
 Detect SBP>250norm (neutrophils)
 Relief abdominal pain and pressure
Contraindication of tapping
 Pregnancy
 Distended bowel
 Distended urinary bladder
 Abdominal wall cellulitis
 Acute abdomen require surgery
 Severe thrombocytopenia & coagulopathy
Mx: ASCITES
 Sodium restriction salt <200mg\mg\d
 Diuretic -spironolactone
 Large volume paracentesis(relief abdominal discomfort,
 Peritoncovenous shunt (leveen shunt &dever shunt)
 Porto system shunt and trasjugular intrahepatic portosystemic shunts(TIPS)
 Liver transplantation

15.Indication of giving normal saline in surgical patients.

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 Flashes wounds and skin abrasions,  TPN

 Dehydration  Tx anaphylaxis
 Resuscitation  Tx shock
 Administer iv drugs  Dysrhythmias
 Administer along with insulin in diabetic  Gastric outlet obstruction
pt  If not sure what to give
 Hypercoagulable state  Fistulas of upper GI,
 Burns  Pancreatic fistula.

16. Management of comatose patient.

Feeding(IV Fluids)
Analgesia
Sedative
Thrombolytic
Head up
Ulcer prophylaxis
Glycemic prophylaxis(give glucose)

Additional:
 O2
 Antibiotic prophylaxis(eg cefotaxime)
 DVT prophylaxis
 Bed sore prophylaxis(pneumatic bed,ripple mattress, change position after every 2 hours)
 Monitor vital signs,monitor urine catheter,
 Give thiamine iv (pabrinex)for wernickes encephalopahthy
 Monitor labs :ABGs,LFTs,Ammonia,Coagulation profile,toxic screen.

17. Types of oxygen mask

 Nasal cannulae- 1-2 l/min, 30-35%.
 Nasal catheter
 simple face mask- 5-6 l/min, 40-60%.
 venturi masks,
 Reservoir bag masks or Non rebreather- 10-15l/min, 80-90%.)
Indications
 Respiratory distress
 shock
 Hypoxemia
 High altitude
 Head injury
 Active contusion ,
 status epileptus
 COPD
 Severe pneumatic respiratory distress
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18.Differentiate breast abscess/mass

MASS- ABSCESS
 Firm  localized breast erythema
 mostly upper outer quadrant,  warmth
 mostly painless  induration,
 skin retraction  Tenderness
 axillary lymphadenopathy  mostly alveolar or periareolar
 peau d'orange.  fluctuance,
 fever.)

19. Classification of dehydration in pediatrics

A. No dehydration
Diarrhea/GE with less than 2 of the following;
 sunken eyes
 return of skin pinch 1-2 secs,
 restlessness/irritability.
Rx, plan A;
 10mls/kg ORS after each loose stool,
 continue feeding.
 Zink supplement(upto 6 1\2 tablet (10 mg)\day for 10-14 days.>6 month 1 tablet (200mg\day for
10-14 days)
 Give advice when to return

B. Some dehydrtion
Able to drink adequately but 2 or more of:
 Sunken eyes,
 Return of skin pinch 1-2 secs,
 Restlessness/irritability.
 Drink eagerly,thirsty
Rx, plan B;
Tx with ORS 4 hour periods
Determine the amount of ORS to give in the first 4 hours according to weight
i. <6kg (200-400ml)
ii. 6-10kg(400-700ml)
iii. 10-12kg(700-900ml)
 ORS by mouth at 75 mls/kg over 4 hours,
 plus, continue feeding as tolerated, reassess at 4 hrs.,
C. Severe dehydration-
Unable to drink or AVPU <A plus;
 sunken eyes,
 Lethargy\unconsciousness

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 return of skin pinch >=2 secs.

 Unable to drink, poorly
Rx, plan C;
Rapid iv infusion,close monitor,followed by ORS once the child improves.
Start with 100ml RL
step 1- 30 mls/kg RL
<12 months for 60 min(1h)
>= 12 months for 30 min .
Step 2; 70 mls/kg RL
<12 months for 5 hours
>= 12months for 2.5 hours .
(If no hospital nearby start rehydration by tube or mouth)
OR ngt rehydration 100 mls/kg ORS over 6 hours.
shock- all four of; weak/absent pulse, AVPU <A, cold hands + temp gradient, capillary refill> 3 secs.
PLUS sunken eyes and slow skin pinch.
Rx,
 RL 20mls/kg over 15 min,
 second bolus may be given if required,
 proceed to step 2 of plan C,
 treat for hypoglycemia,
 start ORS 5 mls/kg/hr once able to drink.)
Signs for over-hydration
i. Tachycardia
ii. Tachypnea
iii. Edema(eyelid)
iv. Tender hepatomegaly
v. Bilateral crepitation
vi. Increase of urine output

20.When to use IV fluids in dehydration

 severe dehydration

21.Types of arteriitis/ phlebitis

 ARTERIITIS- giant cell arteritis, takayasu (aorta) and temporal artery arteriitis, polyartriitis nodosa.
 PHLEBITIS- thrombophlebitis ie superficial vein, DVT)

22.Ectopic pregnancy and differential

This is the implantation of the blastocyst anywhere other than the endometrial lining of the uterus.
Sites of ectopic pregnancy-
a) ampullary
b) isthmic
c) fimbrial/infundibulum
d) ovarian
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e) cornual
f) cervical
g) Abdominal.
Stages of rupture
 Un ruptured ectopic
 Slow leaking
 Acutely rupture
Etiology-
a) Fallopian tube transport malfunction, :
 infections eg chlamydia and gonorrhea,
 previous ectopic pregnancy,
 previous tubal surgery,
 abdominal surgery resulting in adhesions,
 endometriosis,
 congenital abnormalities,
 pregnancy with intrauterine device in place,
b) Assisted reproduction ie ivf, ovulation inducing drugs.
Symptoms-
 amenorrhea,
 vaginal bleeding,
 abdominal pain.
Symptom Ectopic:(9s:
1. Syncope
2. Spotting
3. Shoulder pain
4. Shock
5. Slight anemia
6. Sever LAP
7. Scanty bleeding
8. Secondary amenorrhea
9. Severe abdominal tenderness
Dx.
 US,
 hcg,
 laparascopy.
DDX
1. Ovarian cyst
2. Cystitis
3. Acute pyelonephritis
4. peritonitis
5. spontaneous abortion
6. molar pregnancy
7. choriocarcinoma
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8. cervical cancer
9. appendicitis
10. salpingitis
11. ruptured corpus luteum cyst or ovarian follicle
12. Ovarian torsion
13. urinary tract disease
MX
 Medical-methotraxate IM,
 Surgical- salpingotomy or salpingectomy.)

23.How to manage fetal distress

Fetal distress is depletion of oxygen and accumulation of CO2 resulting from interference with
gaseous exchange and leading to state of acidosis and fetal hypoxia.
Causes-
a) Antepartum causes;
i. Fetal congenital malformatioms,
ii. Cord accidents ie cord tight around the neck compression of cord by baby cord forms a knot,
iii. Obstetric complications i.e utero-placental insufficiency pre-eclampsia/eclampsia malaria in
pregnancy
iv. APH vasa previa placenta previa abruptio placenta,
b) Intrapartum causes;
i. Prolonged/obstructed labour,
ii. Cord presentation/prolapse,
iii. Antepartum haemorrhage.
Dx.
a) detection of abnormal heart rate or rhythm ie fetal tachicardia, fetal bradicardia ,late deceleration,
variable deceleration on CTG.,
b) passage of meconium stained amniotic fluid ic cephlic presentation,
c) biophysical profile score of less than 6/10.
Ddx.
a) breech presentation with passage of meconium,
b) effects of drugs administered to the mother eg tocolytic salbutamol,
c) maternal fever ,hypertension or amnionitis also causes fetal tachicardia.

Mx. Method of choice monitor of fetal during labour intermittent Auscultation using pinnard
stethoscope
if fetal heart rate remains abnormal for 3 consecutive contructions;
a) explain condition and possible complications to the mother,
b) change mothers position left lateral position preferred,
c) stop oxytocin, hydrate with dextrose 5%,
d) give oxygen by face mask
e) examine to rule out predesposing factors,

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f) if in 2nd stage and no malpresentation or severe CPD deliver quickly with the aid of
episiotomy and assisted vacuum delivery,
g) after hydration with at least 1 liter in 30 min and fetal heart rate still abnormal then perform
emergency CS if still in first stage.
Test for fetal well being
a) Fetoscope H.R
b) Doppler ultrasound
c) Palpation of fetal movement
d) HCG test
e) CTG cardiotopography
f) Stress test and non stress test
g) Amniocentesis analysis
h) Fetal kick chart
24.Endemic areas of malaria
a. Endemic; lake victoria and in the costal regions. Annual entomological inoculation rates btw 30-
100.
b. Seasonal transmission; arid and semi arid areas of Northern and South Eastern parts of Kenya.
c. Epidemic prone areas; western highlands of Kenya.
d. Low risk malaria areas; central province and Nairobi.)

25.Management of hematemesis .(MR.BASE)

1. Resuscitation,
2. Medical therapy,
3. Balloon tamponade,
4. Endoscopic hemostasis,
5. Angiotherapy,
6. Surgical hemostasis.
1.Resuscitation;
 Address ABCs,
 Intubate pt to avoid risk of aspiration,
 Using two large bore venous access in the antecubital fossa replace blood loss with cristalloids in
the ratio 1ml blood:3 ml cristalloid,
 Put urethral catheter to monitor urine output. Urine output should be 30-50 ml/hr,
 BP systolic not less than 90mmhg, pulse not more than 120 /min,
 Decrease in urine output and BP suggests need for calloid while decrease in urine output alone
suggests need for cristalloids.
 Insert an NGT and perform an aspirate and lavage procedure.
2. Perform Endoscopy for
Diagnostic purpose
 esophagitis,  esophageal ca,
 esophageal varices,  gastric or duodenal ulcer
 boerhaave tear,  gastric varices,
 mellory weiss tear,  ca stomach,
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 kaposi sarcoma,  foreign body,

 dieulfoy lesion,  coagulopathy,
 A-V malformations,  hemorrhagic gastritis
 angiodysplasia,  aortoenteric fistula,
 Hemophilia,  merkels diverticulum,)
 pancreatic pseudocyst or pancreatic
pseudoaneurism,
Therapeutic purpose
1. vasoactive injection eg epinephrine,
2. sclerosant injection eg absolute ethanol sodium tetradecyl sulphate,
3. band ligation,
4. coaptive coagulation eg thermal therapy) OR:
Determining forrest classification
A. acute Bleeding -
I. spurting hemorrhage,(arterial)
II. oozing hemorrhage(venous)
B. Signs of recent hemorrhage
I. visible vessel (thrombus bleeding)
II. adherent clot,blood clot
III. Hemorrhagic infiltrate on ulcer bottom.
C. clean ulcer(melena or hemoptysis)

3. Medical therapy:
 Gasrtic acid control ie ppi eg omeprazole 40mg,
 H2 blockers eg ranitidine 150mg.
 Vessel constrictorsie somatostatin, octreotide, vasopressin.
 Mucosa protector ie mesoprostol.)
4. Balloon tamponade: sengstaken blakemore tube.
5. Angiography ie embolization.
6. Surgical:
 Truncal vagotomy and pyloroplasty with suture ligation of the bleeding ulcer,
 Truncal vagotomy and antrectomy with resection or suture ligation of bleeding ulcer, proximal
gastric vagotomy with duodenostomy and suture ligation of bleeding ulcer.

26.Pathophysiology of HIV
a) HIV attacks cells with CD4 molecule on their surface e.g T-lymphocytes CD4+ cells, macrophages,
monocytes, dendritic cells.
b) T helpers regulate the proliferation of B cells in response to the presence of a particular antigen.
c) When T helper cell recognizes the presence of the antigen to which it is attuned, it becomes
activated which begins a process that culminates in B cell proliferation and antibody production
towards that particular antigen.
d) By depleting the population of T helpers, HIV renders the body unable to mount an immune
response, leaving it Venerable to bacterial, fungal and viral infections.
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e) After initial infection flu like symptoms develop ie 1-6 weeks afterwards and then clinically
recover.this is the most infectious period due to high volume of circulating virus.
f) CD4 sharply declines until the 6th week when the body's immune system produces antibodies
that fights the virus.
g) CD4 rises but does not reach pre infection level.
h) This is followed by a long period 6-9 years of gradual CD4 decline and viral load increase.
i) As CD4 decreases, chances of acquiring opportunistic infections increase and become more and
more severe.)

27.TB dx and Rx
Dx.
History of presenting complains;
 cough,
 night sweat,
 low grade fever,
 weight loss.
past medical HX;
 diabetes,
 HIV,
 Hx of TB contact
physical examination e.g:
 lymphadenopathy,
 hemoptysis,
 reduced breath sounds on auscultation,
 dullness to percussion,
 hepatosplenomegally,
CXR :
 infiltrates,
 consolidation, or cavities in upper lungs +/- mediastinal lymphadenopathy or pleural effusion, in
milliary tb tiny nodules throughout the lung fields).
Labs:
 sputum AFB microscopy,
 culture,
 molecular test, gene x pert,
 PPD drug sensitivity test.
Rx.
 First line RHZES.
i. Rifampicin(R)-10mg.
ii. Isoniazid(H) -5mg,
iii. Pyrazinamide(Z) -25mg,
iv. Ethambutol(E)-15mg,
v. Streptomycin(S)-25mg)
 New adults: intensive phase:2RHZE
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continuation phase:4RH.
 Pt who relapsed 2SRHZE/1RHZE/5RHE.

28. Uncomplicated and sever malaria

Uncomplicated malaria-characterized by fever in presence of parasitaemia.other features may
include chills, profuse sweating, muscle pain, joint pains, abdominal pain, nausea, vomiting, irritability
and refusal to feed.
Investigations :
Blood slide for mps
Tx of uncomplicated malaria
A. First line TX: uncomplicated malaria \all age
Artemether Lumefantrine(AL)20mg artmether & 120 lumefantrine
Day 1 1st dose 4 tablet
8hours 4 tablet
Day 2 24hours 4 tablet
36hours 4 tablet
Day 3 48hours 4 tablet
60 hours 4 tablet
B. Second line tx: Dihydroartminin piperaquine (DHA_PPQ)
40mg of DHA&320mg PPQ(adult)
20mg of DHA&160mg PPQ(pediatric)

C. Support MX: atripyretic( fever)Eg.paracetamol

IV fluids and nutritions
Severe malaria- life threatening manifestation of malaria. It is detection of p. falciparum in the
peripheral blood.
FORM OF SEVERE MALARIA
(1) Cerebral malaria ie unrousable coma not attributed to any other cause,
(2) Metabolic acidosis with respiratory failure
(3) Alteration in the level of consciousness i.e from drowsiness to deep coma,
(4) Acute Respiratory distress syndrome
(5) Multiple Generalized convulsions ie 2 or more episodes in 24 hours,
(6) Circulatory collapse,Shock, Septicemia,
(7) Pulmonary edema
(8) Abnormal bleeding ie DIC,
(9) Juandice,
(10)Haemoglobinuria (black water fever,)
(11)Acute renal failure ( oliguria or anuria, )
(12)Severe anaemia ie <5g/dl,
(13)Hypoglycemia<2mmol/l,
(14)Hyperparasitaemia
(15)Hyperpyrexia
(16)Fluids and electrolytes disturbance
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Mx:
a) Artesunate :Loading dose 2.4mg\kg\iv
Maintenance dose 1.2mg\kg\24hours
b) Artmeter: Loading dose 3.2mg\kg\IM
Maintenance dose 1.6mg\kg\6hours
c) Quinine :loading dose 20mg\kg in 10ml\kg 5% dextrose over 4 hours(oral dose
10mg\kg\8hours\7days)

29. Colostomy/ ileostomy indication and complication

colostomy: surgical bringing out, through the abdominal wall, a portion of the large intestine to carry
out stool./ exteriorrisation of the large intestine through the abdominal wall to bring out stool.
Indication:
1. Decompress an obstructed colon.
2. Evacuation of stool when the distal colon or rectum is removed due to colorectal ca.
3. To divert the fecal stream in preparation for resection of an inflammatory, obstructive, perforated
lesion or following traumatic injury.
4. To protect a distal anastomosis following resection.

Types of colostomy:
 temporary or permanent.(functional)
 Loop,
 Terminal or End/Hartman
 Double barred (divided/paul-mickulics colostomy)

Care for colostomies:

 Vital signs monitor
 Iv fluids
 Antibiotic prophylactic
 Analgesia
 NPO
 NG tube & catheter monitor input and output

Stroma management;
1. Support the operating site during deep breathing and coughing
2. Observe for color and amount of wound drainage
3. IV fluids and electrolytes until patients diet is gradually resumed
4. Counseling before and after surgery
5. Education to the patient(pouching supply,proper application of pouch to avoid leakage,how to
change pouch,skin care,diet,counseling)

Care After Discharge;

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a) Skin care- clean around the stroma area with soap and water, apply water repellents such as zinc
oxide
b) Odor control
c) Diet- avoid spicy food and take diet rich of roughage
d) Lifestyle
e) Colostomy bags
f) Social support
g) When to consult a doctor
i. stroma color changes
ii. skin irritation for redness or rash
iii. stool change color and amount
iv. Vomiting, abdominal swelling or cramping with fever

Complications of colostomy:
1) Gangrene of stomal tissue.
2) Stomal stenosis.
3) Stomal retraction.
4) Stomal prolapse.
5) Parastomal hernia.
6) Parastormal abscess formation.
7) Infection.
8) Skin irritation around the stoma.
9) Feccal impaction.
10) Diarrhhea.
11) Psycological
12) Bleeding.
Location of colostomy consider:
1. Contour of the abdomen.
2. Away from Belt line, umbilicus and old wound,
3. Away from bony prominences.
4. Place in the descending colon if possible. Semi solid discharge reduces the water loss.

DDX
Colostomies Ileostomies

On the left side On the right side

Shape is flat Shape is sported
Solid fecal Liquid semi solid matter
Larger in size Smaller in size
Low risk of dehydration and electrolyte imbalance High risk of dehydration and electrolyte
imbalance

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Indication of ileostomy
1. Injury of surgical response to disease of larger intestine
2. Disease of large intestines:e.g crohns disease,ulcerative colitis
3. Tx of colorectal cancer

30.Cellulitis dx, ddx & Rx

a) Soft tissue disease of skin and subcutaneous fat
b) Common bacterial skin infection, common group A streptococci or S.aureus
c) Anatomical variants- periorbital, buccal, body piercing, mastectomy, lumpectomy, liposuction,
perianal.
Dx.
 Culture of aspirate and lesions,
 Blood culture,
 Radiology ie XR, CT osteomyelitis, MRI necrotizing fasciitis.
Ddx.
a) Infections;
 Erysipelas
 Necrotizing fasciitis (infection of deep fascia, gas gangrenous eg. c. perfirenges,
 Cutaneous anthrax,
 Vaccinia vaccination (erythema around vaccination point.)
 Lymphadenitis
 Tetanus
b) Inflammatory and neoplasm;
 Insect bite,  Fixed drug reactions,
 Burn  Pyoderma gangrenosa,
 Osteomyelitis  Sweet syndrome acute febrile neutrophilic
 Abscess dermatosis,
 Acute gout,  Kawasakis disease, wells syndrome,
 Acute DVT,  Carcinoma erysipecodies,
 Familial mediterranean fever associated  Raptured bakers cyst.
cellulitis,

Rx.
1. Antibiotics ie cefazolin 1g iv qd, ceftriaxone 1g iv od,
2. Elevation and immobilization of the involved limb,
3. Antifungal i.e imidazole.)

31. Types of chest tube indication ( types of chest tube-

1. Underwater seal drainage.
2. Bileau.
3. Thoracostomy.
4. Malicot.
5. Small bore.
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6. Large bore.
7. Trocar
8. Right angle
9. Flarred
10. Tappered

Indications:
1. Post operative thoracostomy.
2. Pneumothorax.
3. Massive Hemothorax.
4. Chylothorax.
5. Pleural effusion.
Indication of thoracotomy:
1) Cardiac tamponade
2) Initial drainage >1.5L and continuously
3) Hourly drainage >200ml\hr>3hours
4) Electro-cardiac dissociation
5) Intra abdominal bleeding
6) Persistent pneumothorax
7) Diaphragmatic injury
8) Large chest wall defect
9) High velocity injury
10) Impaled object on the chest in situ
11) Trans mediastinal injury
12) Delay findings e.g clotted haemothorax ,lung abscess, or fistula formations
13) Failure of resuscitations measures

Complications:
1. Pneumothorax.
2. Bleeding at the drain site.
3. Infection of insertion site.
4. Accidental disconnection of the system.
5. Accidental drain removal.
6. Unable to remove chest drain.
7. Blockage of the tube.
8.Lung collapse
9.Sepsis
10.Liver injury,spleen,and diaphragmatic lacerations

32. Abdominal incisions

• Kochers, • Lower midline,
• Thoracoabdominal, • Paramedian,
• Upper midline, • Lanz,
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• Gridiron, • McEvedy incisions,

• Pfannenstiel, • Transplanted kidney,
• Muscle splitting loin, • Nephrectomy,
• Gable, • Left inguinal,
• Transverse muscle splitting, • Umbilical port.

33.Pneumothorax
This is the abnormal collection of air or gas in the pleural cavity.
Types
1. Open pneumothorax.
2 Closed pneumothorax.
3.Tension pneumothorax.
4. Spontaneous pneumothorax, primary and secondary.
5. Iatrogenic pneumothorax. Occlusive dressing before tube insertion of open pneumothorax.
In tension pneumothorax:
Flap valve leak develops that allows air in but prevents its escape.
Intrapleural pressure rises, causing total lung collapse and a shift of the mediastinum to the opposite
side.

34.Types of central lines ( these are lines whose tips are located in ivc, spv or right atrium.
Types:
a) Tunneled i.e hickman, groshong, broviac, tunneled dialysis catheter.
b) Non-tunneled ie central lines double triple or quadruple lumen, uldall, quinton catheter.
c) PICC- peripherally inserted central catheters,
d) Implanted Ports e.g single port and double port.N/B swan ganz catheter (tip located in pulmonary
artery)
Indications:
1. Dialysis
2. Administer medicines and fluids
3. Chemotherapy
4. Acute ill pts monitor for CVP
5. Plasma exchange
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6. Long term parenteral nutrition

7. Drugs causing phebitis in peripheral vein(e.g amiodarone,ca+ gluconate)
8. Frequent blood draws
9. Collapse peripheral veins(vessels)

Complications:
a) Acute- arterial puncture,
b) Hematoma,
c) Pneumothorax,
d) Cardiac arrhythmias,
e) Air embolism.
f) Chronic-infection,
g) Catheter thrombosis/DVT,
h) Dislodgement,
i) Central venous occlusion,
j) Catheter fracture,Blocked tube and blood clot
Contraindications
1. Infection
2. Coagulopathy
3. Newly inserted pace maker
4. Renal cell cancer

35.Ddx of hepatosplenomegaly,
Causes of massive spleen ( hepatosplenomegaly )>1000g
Mild 3-5cm
Moderate 5-8cm
Severe >8
A. Infectious:
i. Viral hepatitis (B&C),EBV,CMV,
ii. Leptospirosis,
iii. Toxoplasmosis,
iv. TB,HIV\AIDs,
v. Infectious mononucleosis,
vi. histoplasmosis,
vii. rubella,
viii. Malaria,schistosomiasis,Leishmaniasis
B. Hematological
RBC disease
congenital
1. hereditary spherocytosis
2. hemoglobinopathies
 sickle cell disease,
 thalassemia,
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 enzyme deficiency (pyruvate kinase,G6PD)

Acquired autoimmune
 hemolytic anemia,
 parasitic disease.
Platelet disorders
 idiopathic thrombotytopenic purpura(ITP),
 throbocytopenic purpura(TTP)
Lymphoid disorder
 Non hodgkins lymphoma
Bone marrow disorder (myeloproliferative disorders)
 Myelofibrosis
 Chronic myeloid leukemia
 Acute myeloid leukemia
 Polycythemia vera
C. Storage disease\infiltrative diasease\lysosomal disease
I. Gauchers disease
II. Nieman pick disease
III. Amyloidosis
D. Miscellellaneous disease\lesions
I. Felty syndromes(neutropenia,RA,splenomegaly)
II. Portal HTN(Including right HF)
III. Splenic artery aneurysm
IV. SLE,RA

36. Findings in gynecological examination in elderly

i. Amenorrhea,
ii. Urinary incontinence,
iii. Vaginal dryness and atrophy of vulva
iv. Atrophy of breast
v. Hyperpigmented areolar
vi. Thinning of vagina
vii. Retraction of the cervix
viii. Reduce size of the ovary
ix. Reduce pubic hair
x. Reduce secretion

37.Types of pneumonia and dx.

1) Community acquired,
2) Hospital acquired,
3) Aspiration,
4) Opportunistic pneumonia,
5) Atypical.
Dx.
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Medical Hx.
 Cough,
 fever,
 shortness of breath.
Physical exam.
Inspection
 Tachypnea,
 central cyanosis,
Palpation :Increase in tectile fremitus,
Percussion, :Dullness
Auscultation, :Reduced breath sounds, rales, bronchial breathing.
Labs:
 FHG,
 basic metabolic panel,
 sputum and blood cultures,
 pulse oxymetry,
 ABGs,
CXR :infiltration or consolidation.,
CT chest.

Common agent (Typical CAP.)

i. S.pneumoniae
ii. Haemophilus influenza
iii. S.aureus
iv. Klebsiella
Common agent (Atypical CAP)
i. Mycoplasma pneumoniae
ii. Chlamydia pneumoniae
iii. Chlamydia psittaci
iv. Coxiella burnetti(Q fever)
v. Legionella spp
vi. Viruses:influenza virus(A&B),adenovirus,parainfluenza virus,RVS

38.Respiratory rate in peds

i. > 2 months > 60/min.
ii. 2-11 months > 50 /min.
iii. 11-59 months > 40 /min.

39.DDX and complication of leg ulcers

painfull-
 Arterial ulcers eg emboli/thrombi,
 Artteriosclerosis,
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 Thrombangitis obliterans,
 Hypertensive ulcers,
 Reynaulds disease,
 Vasculitis,
 Scd.
Painless-
 Venous ulcers-  Infectious eg mico bacterial, fungal, parasitic,
 Egvenous occlusion, bacterial.
 Thrombophlebitis.  Neoplasms-scc, basal cell carcinoma,
 Normal vasculature-neuropathic eg DM, sarcoma, lymphoma, metastasis.
 exogenous neurotoxins,  Traumatic-burn, frost bite,
 Alcoholism,  pressure ulcer,
 leprosy,  post radiation,
 Syphilis.  insect bite,
 self induced.
Complications:
 bone and joint,
 cellulitis,
 necrotizing faciitis,
 gangrene,
 sepsis.
Leg examinations
1. Oedema
2. Prominent varicosities
3. Skin discoloration
4. Skin condition colour and temperature
5. Examine calf swelling and tenderness
6. Report pulse dorsalis, pedis, popliteal & femoral pulse to R\O arterial insufficiency
7. Lymphadenopathy inguinal to R\O malignancy ulcer
8. Sensory examination of lower limb to R\O neuropathic ulcer

Etiology of leg ulcer

1) Tropical ulcer(infection is most common)
2) Arterial blood insufficiency to lower limbs
3) Blood disorders e.g sickle cell anemia
4) Neoplasm e.g squamous cell carcinoma
5) Neuropathy e.g associated DM
6) Mixed arterial & venous insufficiency
7) Vasculitis associated with SLE
8) HTN
9) Gross obesity

Venous disease ulcer Arterial disease ulcer

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Shallow usually situated on the guiter area of leg Ulcer with punched out appearance
Edema Base of wound poorly perfused and pale
Eczema Cold legs
Ankle flare Shinny and tent skin
Lipodermatosclerosis Pale or blue feet
Varicose vein Gangrenous toes
Hyperpigmentation

40. criminal abortion

1) Abortion is illegal in Kenya.
2) Grounds on which abortion is permitted are:
 to save the life of the woman,
 to preserve physical health,
 to preserve mental health.
3) Abortion is also illegal if:rape or incest, fetal impairment, economic or social reasons, on request.
4) Abortion is to be performed by a certified physician, with the consent of the woman and her
spouse.
5) Two medical opinions are required: physician and psychiatrist and should be performed in a
hospital. Doctor 14 yrs, woman 7 yrs, other people 3 yrs.)

41. Indication and complication of amputation

indications:
 PVD,
 trauma,
 tumor,
 infection,
 congenital abnormality.
Complications:
 heart complications,
 venous thrombosis,
 wound infections,
 pneumonia,
 phantom limb pain,
 psychological problems.

42. What to check for in patient with pleural effusion

Lab Tests to order are:
1. Fluid and serum protein,
2. Glucose,
3. LDH,
4. Fluid culture and gram stain,
5. Fluid cytology and cell count with differentials,

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6. fluid amylase
7. AFB, ANA, RF, PH.
A. Transudate:
i. Appearance is clear,
ii. Specific gravity is <1.012,
iii. Protein content is <2.5g/dl,
iv. Fluid protein/serum protein <0.5,
v. Fluid LDH /serum LDH <0.6, LDH <200,
vi. Glucose > 60,
vii. Cholesterol content <45mg/dl.
Causes:
 CHF,
 Liver cirrhosis,
 Hypoproteinemia,
 Nephrotic syndrome,
 Acute atelectasis,
 Myxedema,
 Peritoneal dialysis,
 Meigs syndrome,
 Obstructive uropathy,
 End stage kidney disease.
B. Exudate:
i. Appearance is cloudy,
ii. Specific gravity is > 1.020,
iii. Protein content > 3.0g/dl,
iv. Fluid protein/serum protein > 0.5,
v. Fluid LDH/serum LDH > 0.6, LDH >200, glucose <60,
vi. Cholesterol content > 45mg/dl.
Causes:
 Malignancy,
 Infection,
 Trauma,
 Pulmonary infarct,
 Pulmonary embolism,
 Autoimmune disorders,
 Pancreatitis,
 Boerhaave syndrome,
 Rheumatiod pleurisy,
 Drug induced lupus,
 Tuberculosis.

43. Causes and investigation in Gangrene

Tissue necrosis because of poor vascular supply or severe infection ie c. perfirengens.
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Types:
1. Wet - dead tissue+infection
2. Dry - dead tissue no infection,clear margins
3. Gas - infected muscle with clostridium perfirenges + gas +necrosis
4. Fourniers gangrene -perineal gangrene
Causes;
i. C.perfiregens,
ii. Diabetes mellitus,
iii. Artherosclerosis,
iv. Peripheral vascular disease,
v. Smoking,
vi. Trauma or serious injury,
vii. Raynauds phenomenon.
viii. Others :drugs,obesity,age,immunodepression,
Characteristic of gangrene
1) No bleeding
2) Dark colour changes
3) Absent of sensitivity
4) No mobility
5) Low temperature
6) Foul smelling (in gas gangrene)
Dx. H/P:
1. Prior skin infection or penetrating wound,
2. Severe pain in skin,
3. Skin crepitus,
4. Rotten smelling skin.
Investigations;
I. FHG,
II. Blood sugar,
III. Culture of tissue or fluid from wound,
IV. ABGs,
V. Xray, CT scan, MRI.
VI. Angiography
VII. Ultrasound \doppler
Tx:
1. Revascularization
2. Hyperbaric chamber
3. Debridement
4. Amputation
5. Antibiotic cover

44. how to manage nose bleeding (Epistaxis)

Causes:
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 Trauma
 Mucosal irritation(e.g foreign bodies)
 Septal abnormalities
 Polyps
 Infection
 Tumor and Masses

First aid:
1. Ask pt to sit down and firmly pinch soft part of the nasal cavity above the nostrils for 10 min,
2. Pt should lean forward and breath through the mouth this will drain down the nose instead of
down the back of the throat,
3. Pt should stay upright rather than lie down as this will reduce blood pressure in the veins of the
nose, Maintain pressure on the nose for up to 30 min to allow for blood clotting,
4. Place a covered ice pack on the bridge of the nose, avoid blowing the nose , bending down and
strenious activity for at least 12 hours after a nose bleed.

Medical Management:
I. ABCs
II. Determine site of bleeding
III. Adequate sanction
IV. Adequate pain control,
V. Ballooning
VI. Nasal packing:Types Anterior&Posterior
VII. Further test e.g coagulation profile,
VIII. Give Antibiotics,
IX. Give vasoconstrictors (e.g epinephrine)
X. Surgical management for recurring nose bleeds e.g septal surgery, cautery, ligation)

45. Types of hepatitis

a) Viral e.g A, B, C, D, E,
b) Drug induced hepatitis,
c) Alcoholic hepatitis,
d) Autoimmune hepatitis.)

46. Indication and Complication of Splenectomy

Types splenectomy: open & laparoscopic
Indications
1. Splenomegaly that destroys platelets and red blood cells i.e CLL, CML,chediak Higashi syndrome ,
gaucher disease,
2. Lymphoma diagnosis,
3. Wandering spleen,
4. Idiopthic thrombocytoenic purpura(ITP)
5. Trauma,
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6. Spontaneous rapture,
7. Spread of gastric ca to spleen,
8. Pyruvate kinase deficiency,
9. B-thalasemia,
10. Hereditary spherocytosis,
11. Felty syndrome(neutropenia, RA, splenomegaly)
12. Myelodysplastic syndrome.

Complications;
a) Overwhelming post splenectomy
b) Sepsis OPSS,
c) Missed accessory spleens,
d) Portal vein thrombosis,
e) Pancreatic tail injury leading to abscess and fistula,
f) Thrombocytosis, bleeding,
g) Wound infection,
h) Changes in peripheral smear i.e
a. Howell-jolly bodies (nuclear fragments),
b. Heinz bodies (hemogobin deposits),
c. Pappenheimer bodies (iron deposits),
d. Target cells, spur cells (acantocytes),
i) Increase of platelets and leucocytes count post splenectomy.
Vaccination post splenectomy
1) H.influenza vaccine
2) Pneumococcal vaccine
3) Neisseria vaccine
4) Malaria prophylactic
5) Antibiotic prophylactic

47. causes of stroke

Hemorrhagic:
 Hypertensive crisis,60%
 Eclampsia,
 Aneurism,
 Trauma.
 Cocaine use
 Vasculitis
 Thrombolytic therapy
 Anticoagulant therapy
 Intracranial aneurysm
 Intracranial neoplasm (bleeding from brain tumor)
 Advance Age

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Ischemicie thrombotic or embolitic:

 Malignancy,
 MI
 Smoking
 Endocarditis,
 Hypotension,
 Diabetes melitus,
 Cardiac diseasesie (atrial fibrilation, heart failure, mitral stenosis),
 Carotid stenosis,
 Hyperhomocystinemia.
 Atherosclerosis
TIA:
 Carotid stenosis,
 Lifestyle e.g alcohol,
 Inactivity,
 SCD,
 Oral contraceptives,
 Postmenopausal hemorrhage.

48. Lifecycle of Malaria

1.Infected female anopheles mosquito inoculates sporozoites into the human host.
2.The sporozoites infect the liver cells (3-16 days) matures into schizonts.
3.The schizonts then ruptures and releases merozoites.
4.The merozoites infect the red blood cells mature into trophozoites.
5.The ring stage trophozoites mature into schizonts which rupture and release merozoites.
6.The merozoites then differentiate into gametocytes.
7.The gametocytes, male (microgametocytes) and female (macro gametocytes) are ingested by
anopheles mosquito.
8.In the anopheles mosquito stomach, the microgametes penetrate the macrogametes and generate
the zygotes.
9.The zygotes become motile and elongated to form ookinetes.
10.The ookinetes invade the midgut ofthe mosquito and develop into oocysts.
11.The oocyts grow rupture and release sporozoites.

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49. Indication, contraindication of lumbar puncture

A needle is introduced into the subarachnoid space btw L3 and L4vertebrae, usually to obtain a
sample of CSF for diagnostic purpose.
Indications:
A. Diagnostic:
1. Signs of meningeal irritation +/- fever eg meningitis or subarachnoid hemorrhage.
2. Unexplained Fever with disturbed counciousness.
3. Unexplained coma.
4. Myelography.
5.Suspected neurological diseases (guillain barre syndrome, acoustic neuroma, multiple sclerosis,
nervous system involvement in lyphomas and leukemias.)
6.CNS involvement in lymphoma & leukemia.
B. Therapeutic:
1. Spinal anaesthesia. & analgesia
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2. Admin Intrathecal chemotherapy (methotrexate)

3. Treatment of elevated ICP in cryptococcal meningitis.
Contraindications:
1. Papilledema.
2. Local sepsis.
3. Hypotension.
4. Bleeding/cloting disorders.
5. Vertebral deformities eg scoliosis or kyphosis.
Complications:
1. Introduction of infection.
2. Transtentorial or tonsilar herniation.
3. Low pressure headache.
4.bleeding
5. Cerebral herniation
Ddx btw traumatic lumbar puncture and subarachnoid hemorrhage.
1. CSF is hemorrhagic, if it clears it it traumatic, if it doesnot clear it is subarachnoid hemorrhage.
2. In Subarachnoid hemorrhage, supernatat of the centrifuged CSF becomes yellow, ie xanthochromia.

50. DVT Dx DDx and Rx

virchows triad: stasis, hypercoagulable states, endothelial damage.
Dx:
 Coagulation profile,
 D-Dimer testing,
 Ultrsonography,
 Venography,
 Impendance plethysmography,
 MRI, nuclear imaging,
 wells score.
DDx:
1. Baker cyst,
2. budd-chiari syndrome,
3. cellulitis,
4. congestive heart failure,
5. pulmonary embolism,
6. septic thrombophlebitis,
7. superficial thrombophlebitis,
8. cellulitis,
9. muscle damage,
10. external venous compression,
11. lymphedema.
Rx.
1. Anticoagulation ie Heparin 10,000 iv
2. LMWH,
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3. Warfarin,10mg start (3days)

4. Monitor INR 2-3 stop heparin
5. Rivarixoban,
6. Compression TED stocking,
7. Exercise(Immolization)
8. Elevation of the limb,
9. IVC filters.
Prevention
I. Prophylaxis heparin in bedridden pts-5000iu
II. Early mobilization post surgery
III. Prophylaxis heparin in high risk surgery
IV. Lifestyle changes\stop smoking\lose weight\
V. Vena cava filters

51. How to check for pallor

1) Palms,
2) Nails,
3) Lower conjuctiva,
4) Lips,
5) Tongue,
6) Mucous membranes.

52.Management complication of bedridden patients (FAST HUG)

Mx.
1. Pts lie in lateral position, change position 2 hourly,
2. Tap pts back after changing posture with palm for 1 min to remove any saliva or mucus in the
throat or chest to prevent pneumonia,
3. Apply spirit and powder on the back and buttocks twice daily,
4. Make pt sit for 1-2 hours with help of pillows,
5. Air or water filled mattresses can be used.
6. Urine catheters should be changes every 2-3 weeks.
7. Pts should pass stool every 1-2 days, use bed pan for stools,
8. In case of constipation lax like syrup should be given,
9. Physiotherapy of paralyzed limbs should be done twice daily,
10. Daily mouth cleaning with saline water and if possible tooth brushing should be done,
11. Pts be sponged with lukewarm water daily do clean underarms and genitals.

Complicationin bedridden patient

 DVT
 Ulcers
 Aspiration pneumonia
Bedsore sites
 Ischial tuberosity
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 Sacral region
 Patellar
 Forehead.nose,chin
 Scapula

SHEA Grading of bedsore

Stage 1 blanchable erythema that resolve 1 hour after pressure relief ,skin intact
Stage 2 a partial thickness loss of skin
Stage 3 full thickness loss of skin
Stage 4 represent extension into muscle,bones,tendon or joint capsules.

Causes of bedsores
1. Impaired mobility
2. Contracted spasticity
3. Inability to perceive pain
4. Poor skin quality,old age
5. Incontinence (urine and fistula)
6. Bacterial contamination
7. Malnutrition
Tx: Bedsore
Relieve pressure (every 2 hours turning and repositioning after)
Wound dressing tropical

53. Causes of surgical jaundice

common causes:
 Common bile duct stones,
 Carcinioma of the head of the pancreas,
 Malignant porta hepatis lymph nodes.
Infrequent causes:
 Ampullary carcinoma,
 Pancreatitis,
 Liver secondary.
Rare:
 Benign strictures eg iatrogenic or trauma,
 Recurrent cholangitis,
 Mirrizi's syndrome,
 Sclerosing cholangitis,
 Cholangiocarcinoma,
 Billiary atresia,
 Choledochal cysts,
 Parasitic infections.

54. Indications and types of IV fluids

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Type:
 Cristaloids: N saline, RL, Hartman solution, Dextrose 5%, 10%, 40%.
 Colloids: Dextran, gelatin,albumin,
 Blood products: Fresh frozen plasma, Cryoprecipiatae, Blood, Packed Cells.
Indications:
NS:
I. Volume deficits ie in hemorrhage, severe vomiting or diarrhea, heavy drainage from GI suction,
fistulas or wounds,
II. Shock,
III. Mild hyponatremia,
IV. Metabolic acidosis eg DKA, e)resuscitation,
V. Used with administration of blood products.
RL:
I. Diarrhea or vomiting,
II. Fistula drainage,
III. Fluid loss due to burns and trauma,
IV. Hypovolemia due to third space shift.
ALBUMIN 5%:
I. Volume expansion,
II. Moderate protein replacement,
III. Achievement of hemodynamic stability in shock state.
Calculate maintainace therapy= 4/2/1 rule, weight+40= rate ml/hr.

55. Total parenteral nutrition indications and contraindications

Indiction:
 Eterocutaneus fistula,
 moderate/severe malnutrition,
 acute pancretitis,
 abdominal sepsis,
 prolonged ileus,
 major trauma and burns,
 severe inflammatory bowel disease.
Complications:
 Infection,
 Blood clots,
 Liver failure,
 Hunger,
 Hypokalemia,
 Hyponatremia,
 Hypercholoremia,
 Deranged LFTs,
 Trace elements and folate deficiency,
 Lenoleic acid deficiency.
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56. How to diagnose and treat hemothorax

Medical Hx:
 Hx of trauma,
 Chest pain,
 Dyspnoe,
 Tachypnoe,
 Tachycardia,
 Hypotension,
 Diminished ipsilateral breath sounds,
 Dullness to percussion.
Labs:
 Thoracentesis hemorrhagic,
 Pleural fluid analysis.
Imaging:
 CXR, ultrasound, CT.
Rx.
 Goal is to stabilize pt ABCs,
 Stop the bleeding,
 Remove blood and air from pleural cavity. Insert chest tube or do thoracotomy.
 Treat underlying course.
Complications:
 Atelectasis,
 Fibrosis,
 Infection,
 Shock.

57.Indication for intraosseous line

 Difficulty in establishing venous access i e burns,
 Obesity,
 Edema,
 Seizures.
 Necessity for high volume fluid infusion ie hypovolemic shock,
 Burns.
 Access to systemic venous circulation ie cardiopulmonary arrest, burns, blood draws, local
anesthesia, Medication Infusion. Maximum for 8 hours)

58.Head trauma
Anatomy:
S-Skin,
C-Connective tissue,
A -Aponeurosis of galea,
L-Loose areolar tissue,
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P-Pericranium
Skull-
a) the calvarium layers i e outer table, diploe, inner table,
b) base of the skull.
Meninges: laceration of middle meningeal artery causes epidural hematoma, bleeding from the dural
venous sinuses causes subdural hematoma.
Brain: cerebrum, brain stem and cerebellum.
Tentorium: the tentorium cerebri divides the head into the supratentorial compartment ie anterior
and middle fossae and the infratentorial compartment ie posterior fossa with the midbrain connecting
the cerebral hemispheres to the rest of the brain stem through the tentorial incisura.
The midde part of the temporal lobe ie the uncus, usually hernites through the tentoril notch, uncal
herniation causing compression of the;
a) midbrain reticular activating system thus depressed level of counciousness,
b) occulomotor nervecausing ipsilateral pupillary dilatation and loss of pupillary light reflex,
c) cortical spinal tract causing contralateral hemiplegia. So intracranial hematoma causes ipsilteral
pupillary dilatation and contrlateral hemiplegia but in 25% of cases, mass lesion my push to the
opposite side and cause ipsilateral hemiplegia ie kernohan notch syndrome.
CSF: normal ICP is 0-10 mmhg ie 13.6 cmH2O.
Monroe kellie doctrine:
(The total volume of intracranial contents must remain constant.)
 1400g of brain,
 75ml of blood
 75ml of CSF,
 cerebral perfussion pressue is MAP-ICP=70mmhg. MAP=DBP+1/3 pulse pressure.
Classification of head injury:
a) mechanism of injury; blunt ie high velosity eg RTA, low velosity eg fall or assault, and penetrating ie
gunshot wound, other penetrating injuries.
b)Severity; mild ie GCS 13-15, moderate ie GCS 9-12, severe ie GCS 3-8.
c) Morphology;
i) skull fractures ie vault eg open or closed, depressed or non depressed, linear or stellate. Basilar ie ie
+/- CSF leak, +/-CN VII palsy.(O/E racoon eyes, battle sign, rhinorrhoea, otorrhoea)
ii) intracranial lesions ie focal/hematomas e.g epidural (O/E lucid interval), subdural,
intracerebral/contusion recovers in 1-2 weeks.
Diffuse/parenchymal ie mild concussion ( O/E confussion and disorientation without loss of memory,
classic concussion (O/E LOC <6 hrs, amnesia and post concussion syndrome) and diffuse axonal injury
(O/E prolonged post traumatic coma).
d) 1º or 2º brain injury, 1º brain injury occurs due to the initil traumaand cant do anything about it, 2º
brain injury ie complications after 1º brain injury e.g cerebral edema, intracranial hematomas, hypoxic
ischemia, infections in penetrating injuries, epilepsy, hydrocephalus, pneumocephalus.
Management:
 Primary survey ie ABCDE,
 secondary survey ie head to toe examination.
Indications for hospital admission:
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 All penetrating head injuries,

 skull fractures,
 CSF leak,
 moderate to severe headache,
 alcohol or drug intoxication,
 LOC, amnesia,
 significant ssociated injury,
 no CT scan available,
 abnormal CT scan,
 No reliable companion at home,
 unable to return promptly.

59. Chest trauma

1. Massive hemothorax,
2. Open pneumothorax
3. Closed pneumothorax
4. Tension pneumothorax
5. Flail chest,
6. Cardiac tamponade

Life threatening chest injuries;

1. Airway obstruction-
Exam:
1. anxiety,
2. stridor,
3. hoarseness,
4. altered mental status,
5. apnoe cyanosis.
Rx. Intubate, remove foreign body with laryngoscope before intubation if possible.

2. Tension pneumothorax-
Clinical DX: one way valve causing accumulation of air in pleural space.
Exam:
1. respiratory distress,
2. distended neck veins,
3. cyanosis,
4. asymmetry of chest wall motion,
5. tracheal deviation away from pneumothorax,
6. percussion hyperresonnance,
7. unilateral absence of breath sounds.
Rx. Needle thoracostomy- large bore needle, 2nd ICS mid clavicular line, followed by chest tube in
5th ICS anterior axillary line.
3. Open pneumothorax-
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Air entering chest from wound rather than trachea.

Exam:
1) penetrating wound 2/3 of tracheal diameter,
2) unequal breath sound.
Labs: ABG decreased.
Rx. Air tight dressing sealed on 3 sides, chest tube, surgery.

4. Massive hemothorax-
> 1500cc blood loss in chest cavity.
Exam: pallor, flat neck veins, shock, unilateral dullness, absent breath sounds, hypotension.
Investigations: CXR supine- entire lung appears radiopaque as blood Spreads out over posterior
thoracic cavity.
Rx. Restore blood volume, chest tube, thoracostomy if > 1500cc total blood loss or > 200 cc/hr
continued drainage.

5. Flail chest:
free floating segment of chest wall due to > 2 rib fractures each at 2 sites, underlying lung contusion.
Exam: paradoxical movement of flail segment, palpable crepitus of ribs, decreased air entry on
affected side.
Investigations: ABG- decreased pO2 and increased pCO2, CXR- rib fractures, lung contusion.
Rx. O2+fluids+pain control, positive pressure ventilation, intubation and ventilation.

6. Cardiac tamponade-
Clinical dx, pericardial fluid accumulation impairing ventricular function.
Exam:
1. penetrating wound,
2. becks triad (hypotention, distended neck veins, muffled heart sounds),
3. tachycardia,
4. tachypnoe,
5. pulsus paradoxus,
6. kussmauls sign (increased JVP on respiration.)
Investiagtions: echocardiogram, FAST.
Rx. IV fluids, percardiocentesis, open thoracotomy.

60. Hyperkalemia, Hypokalemia

Hypokalemia-<3.5meq/l.
Symptoms-
1) Muscle weakness,
2) Cramps,
3) Ileus,
4) Rhabdomylysis,
5) Arrhythmia.
6) Ecg-ST depression, T wave inversion, prominent U wave, QT prolongation
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Etiology:
GI losses
i. Vomiting and nasogastric drainage
ii. Diarrhea
iii. Laxative and enemas
iv. Intestinal fistulas
v. Decrease k+ absorption in intestinal disorders
Renal losses
i. Diuretics
ii. Renal tubular and parenchymal disease
iii. Primary and secondary hyper aldosteronism
iv. Excessive glucocorticoids
v. Magnesium def
vi. Bartters syndrome(hypokalemia,metabolic alkalosis,BP normal or Low)
Others causes:insufficiency from diet,insulin administer,epinephrine
Diagnosis;
 Hx of etiology eg diarrhea, Diuretics,
 Check magnesium,
 Acid base status,
 k+ serum and urine,
 ECG.
Rx.
Treat causes,
oral KCl most pt 40 meq q2-4 hrs.I
V KCl NPO 10 meq/hr periphery or 20 meq/hr centrally.

Hyperkalemia- > 5.5. > 6.5.

Symptoms-
1. Muscle weakness,
2. Cardiac conduction abnormality,
3. ECG-K+ 5.5-6.5 tall peaked T waves. 6.5-8 QRS widens, BBB, AV block. 8-10 P wave flatens, > 10
sine wave.
Etiology:AAARRRTTT
i. ACE inhibitor
ii. Addison disease
iii. Artifact (iatrogenic overdose)
iv. Rhabdomyolisis
v. Renal tubular acidosis
vi. Renal failure
vii. Tran-cellular shift
viii. Tumor lysis syndrome(K+ release from cells lysis i.e cell lysis)
ix. Treatment(rapid administer of b blockers)

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Diagnosis:
I. Evaluate renal function,
II. Evaluate hypo-aldosteronism.
Rx:
1. Treat etiology,
2. Transient treatment eg IV ca+,
3. Sodium bicarbonate increase PH which shift the k+into the cell
4. insulin + glucose, b 2 agonist (albutrrol),
5. Remove K+ from body(sodium polystyrine sulfonale i.e kayexalate,
6. Diuretics e.g loop and thiazides,
7. Dialysis..(hemodialysis)

61.Cancer of – cervix, ovary, pancreatic, gastric, prostate, esophageal

A. Esophageal cancer:
squamous cell carcinoma(most common) and adenocarcinoma.
Risk factors:
 SCC- alcohol and tobacco use.
 Adenocarcinoma: barrets esophagus ie columnar metaplasia of the distal esophagus secondary to
chronic GERD and obesity.
H/P:
1. Progressive dysphagia ie initially solids then solids and liquids,
2. Weight loss,
3. Odynophagia,
4. Reflux,
5. GI bleeding,
6. Vomiting,
7. Weakness,
8. Cough,
9. Hoarseness.
Labs: EGD with biopsy used to make a diagnosis.
Radiology:
a. barium swallow shows narrowing of the esophagus and abnormal mass.
b. MRI, CT, PET used to determine extension of metastases.
Rx.
a) Surgical resection ie total esophagotomy for early stage of the disease,
b) radiation and chemotherapy used in join operative cases or neoadjuvant therapy to surgery.
Complications:
I. poor prognosis,
II. local extension
III. metastases are frequently present by time of diagnosis.

B. Gastric cancer:
Adenocarcinoma(common) and squamous cell carcinoma.
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Types:
a) ulcerating resembling ulcers seen in PUD,
b) polypoid: large intraluminal neoplasms,
c) superficial spreading: mucosal and submucosal involvement only, best prognosis,
d) linitis plastica: all lyers of stomach involved, decreased stomach elasticity, poor prognosis.
Risk factors:
I. H. pylori,
II. family hx,
III. tobacco,
IV. japanese,
V. alcohol,
VI. vit C deficiency,
VII. high consumption of preserved food,
VIII. males> females.
H/P:
a. weight loss,
b. anorexia,
c. early satiety,
d. vomiting,
e. dysphagia,
f. epigastric pain,
g. virshows node,
h. sister mary joseph node.
Labs:
I. incresed carcinoembryogenic antigen CEA,
II. increased 2-glucuronidse in gastric secretions,
III. anemia if active bleeding,
IV. EGD with biopsy used for diagnosis.
Radiology:
barium swallow may show mass or thickened lether bottle stomach.
Rx.
i. subtotal gatectomy for lesions in distal 1/3 of stomach,
ii. total gastrectomy for lesions in middle or upper stomach or invasive lesions,
iii. adjuvant chemotherapy and radiation therapy.

C. Exocrine pancreatic cancer:

most common adenocarcinoma of the head of the pancreas.
Risk factors:
a) chronic pancreatitis,
b) DM,
c) family hx,
d) tobacco,
e) high fat diet,
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f) male> female,
g) obesity,
h) sedentary lifestyle.
H/P:
I. abdominal pain radiating to the back,
II. anorexia,
III. nausea,
IV. vomiting,
V. Weight loss,
VI. fatigue,
VII. steatorrhea,
VIII. jaundice if bile duct obstructed,
IX. palpable non tender gall bladder (courvoisier sign),
X. splenomegaly,
XI. palpable deep abdominal mass,
XII. ascites.
Labs:
i. possible hyperglycemia,
ii. increased CEA and CA-19-9 tumor markers,
iii. increased total and direct bilirubin,
iv. Increased alkaline phosphate with bile duct obstruction,
v. biopsy used to make diagnosis.
Radiology:
I. CT shows mass,
II. dilated pancreas,
III. local spread and dilated bile ducts.
IV. US usefull for imaging mass.
V. ERCP locates tumor not seen on CT.
Rx.
1. Non metastatic disease limited to the head of pancreas may be resected with Whipple's
procedural removal of pancreatic head, duodenum, proximal jejunum, common bile duct,
gallbladder and distal stomach.
2. Lesions in body or tail are rarely amenable with surgery but can be resected via subtotal
pancreatectomy if found early.
3. Adjuvant chemotherapy is useful.
4. Stenting of pancreatic ducts, billiary ducts, or duodenum can be performed as palliative therapy in
advanced disease.
Complications: migratory thrombophlebitis i.e trousseu syndrome.

D. Prostate cancer:
adenocarcinoma occurring in peripheral zone of prostate.
Risk factors:
 increased age,
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 familial hx,
 high fat diet,
 Prostatitis.
H/P:
a. frequently asymptomatic,
b. weakened urinary stream,
c. urinary retention,
d. weght loss,
e. back pain,
DRE-
a) prostate enlargement,
b) asymmetry,
c) median sulcus obliterated,
d) fixity of prosate mucosa and the overlying rectal mucosa,
e) nodularity,
f) woody hard prostate,
g) tenderness,
h) blood in the examination finger.
Labs:
a. urinalysis may show hematuria and pyuria.
b. increased PSA,
c. increased alkaline phosphate,
d. biopsy provides diagnosis.
Radiology:
• transrectal US shows irregular prostate, bone scan,
• CXR and CT may detect metastases.
Rx.
a) Good prognosis with early treatment,
b) radical retropubic, perineal, laparascopic or robotic prostatectomy.
c) Radiation therapy using external beam radiation or brachytherapy,
d) monitor PSA postmastectomy, antiandrogen therapy/orchidectomy may be used.
Complications: incontinence and impotence.

E. Ovarian tumors:
benign ovarian tumors:
1. follicular cyst,
2. corpus luteum cyst,
3. mucinous or serous cystadenoma,
4. endometrioma,
5. benign cyst teratomaie desmoid cyst
6. stromal cell tumor.
Ovarian cancer:
Stages of ovarian ca:
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I. Ovary only in 1or2 ovaries

II. Extended beyond pelvic and ovaries
III. Extended to the peritoneal cavity
IV. Extended beyond the peritoneal cavity and distant metastases
• mostly epithelial or germ cell in origin.
• Mostly diagonised after considerable growth.
Risk factors:
1. family hx,
2. infertility,
3. nulliparity,
4. BRCA1 or BRCA2 gene mutations.
H/P:
1) usually asymptomatic till late in disease course.
2) Abdominal pain,
3) fatigue, weight loss,
4) change in bowel habits,
5) menstrual irregularity,
6) ascites, palpable mass.
Labs:
increased CA-125in epithelial tumors, alfa fetoproteins, hcg and LDH may be increasedin germ cell
tumors.
Radiology:
• US used to detect mass,
• MRI or CT used to stage the disease.
Rx.
a) Epithelial tumors:
1.TAH/BSO, pelvic wall sampling and appendectomy, adjuvant chemotherapy frequently prescribed.
2. Tumor debulking with resection of involved bowel, liver, omentum, spleen and lymph nodes
perfomed fo extensive disease with metastases.
3. Single oopherectomy may be performed for tumors detected early and pt wants to maintain
fertility. b) Germ cell tumors:
1. Unilateral oopherectomy performed for limited disease.
2. Surgical debulking performed for extensive disease.
3. Chemotherapy postopp.
Complications: prognosis is poor as disease is frequently detected late.

F. Cervical cancer:
bethesda classification of cervical squamous cell dysplasia and appropriate therapy:
1. atypical squamous cell of undetermined significance(ASCUS),
2. atypical squamous cell cannot exclude HSIL (ASCH),
3. low grade squamous intraepithelial lesion (LSIL)/CIN 1,
4. high grade squamous intraepithelial lesion (HSIL)/CIN 2 or 3,

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5. squamous cell carcinoma. Dysplasia progresses to squamous cell carcinoma, adenocarcinoma or

adenosquamous carcinoma.
Risk factors:
1. early first intercourse,
2. tobacco,
3. HPV type 16, 18, 31 and 33,
4. multiple sexual patners,
5. high risk sexual patners,
6. hx of STD.
H/P:
1) usually asymptomatic in early stages,
2) possible vaginal bleeding i.e postcoital or spontaneous,
3) pelvic pain,
4) cervical discharge,
5) cervical mass may be palpated,
6) invasive ca seen on examination.
Labs:
1. pap smear,
2. punch biopsy of visible lesions,
3. cone biopsy determines extent of invasion.
Radiology; CT, MRI, US to determine extent of disease.
Rx. Treat cellular dysplasia. Conization, TAH or radiation therapy used depending on stage of the
disease.

62.Enterocutaneus fistula
Fistula is an abnormal tract btw two ar more epithelial lined surfaces.
ECF is btw bowel and skin.
Classification: several ways to classify are
1. Descriptive ie site of origin and termination eg ECF,
2. Anatomical classification:
stages-serra classification,
Type 1 esophageal, gastric or duodenal fistulas,
Type 2 small bowel fistulas,
Type 3 large bowel fistulas,
Type 4 all of the above drain through one large abdominal defect.
3. Internal vs external.
4. Physiological classification:
I. Low output ()<200ml in 24 hrs,
II. Moderate output (200-500 ml in 24hrs,)
III. High output (> 500 ml in 24hrs. )
5. Etiolgical :
 spontaneous or iatrogenic.
6. Charecteristics of the tract ie simple or complex .
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7. End or lateral fistulas.

Causes of ECF:
1. iatrogenic,
2. trauma,
3. foreign body,
4. crohns disease,
5. infectious diseases eg TB,
6. malignancy.
Tests that predict mortality in ECF:
I. serum transferin,
II. Retinol binding protein,
III. Thyroxine binding pre-albumin.
Rx.
1) Phase 1: recognition and stabilization.
2) Phase2: anatomical defination and decision.
3) Phase 3: definitive operation.
4Rs of fistula management:
1) Ressupitation,
2) Restitution,
3) Reconstruction,
4) Rehabilitation.
Complications: fluid and electrolyte imbalance, malnutrition, sepsis, wound excoriation.

63.Management of intestinal obstruction

Initial conservative mx:
i. Nasogastric tube for decompression
ii. Iv fluid dehydration
iii. Catheterization monitor input and output
iv. Visualization of foreign materials
v. Antibiotic prophylaxis
vi. Soapy enemas used for partial distal obstruction
Surgical mx:
Indications
1. Peritonism
2. Continued deterioration of general condition of patient
Procedures:
a) lysis of adhesion,reduction of intussusception,vulvulus,incercerated hernia.
b) Enterotomy with removal of bezoars foreign bodies gallstones
c) Resection of bowel for obstructing lesion,strangulation bowel.
d) Bypass of intestine around the obstruction
e) ECF proximal to obstruction:colostomy.cecostomy

64. Neck masses 3T (thyroid, thyroglossal cyst, thymus) and how to differentiate them
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DDX of neck mases:

Duration <3week infection
Long duration lymph nodes \neoplasm
Midline mases:( move with the larynx upon swallowing, they include:)
I. dermoid cyst, <2years old
II. thyroid nodule
III. thyroglassal duct cyst. Below hyoid
IV. Chondroma >20 years,bony hard
Submandibular triangle
i. Malignant lymphadenopathy
ii. TB lymphadenitis firm or non tender
iii. Salivary gland pathology
Anterior triangle
i. Branchial cyst
ii. Carotid artery aneurysm
iii. Carotid body tumor
Posterior triangle
i. Cystic hygroma (infant)
ii. Subclavian artery aneurysm
Lateral neck mases include:
i. Enlarged lymph nodes,
ii. Abscess,
iii. Sebaceous cyst,
iv. Lipoma,
v. Submandibular gland,
vi. Brachial cyst,
vii. Sternomastoid tumor.
Note;
if the mass is firm/soft,
any change in size,
tender,
Duration,
any other associated symptoms.
Causes of cervical lymph node enlargement:
1. bacterial ie streptococcal, TB, cat scratch fever,
2.viral ie infectious mononucleosis, herpes simplex, rubella, pharyngitis, HIV,
3. malignant ie lymphomas, thyroid, oral metastases.

65. Paraplegia, paraparesis

1. Paraplegia is impairment of motor or sensory function of the lower extremities.
Causes: spinal cord injury, congenital abnormality eg spina bifida.
2. Paraparesis: is partial paralysis of the lower extremities.

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66. Cervical collar (Philadelphia)

Neck brace..it is an orthopedic medical device used to support a pts neck and head.
Indications;
1) nerve root irritation,
2) stable/simple fracture,
3) reduced dislocation.

67. Pneumonia types, severity, diagnosis and management

Types:
1. Community acquired,
2. Hospital acquired,
3. Aspiration,
4. Opportunistic pneumonia,
5. Atypical.
Curb-65
Pneumonia severity score:
C:Confusion,GCS1point.
U:urea,BUN>191point.
R:respiratory rate>301point.
B:BP<90/601point.
65:age>651point.
0-1 point low risk.
2-5 points high risk
Dx.Medical
1. Hx.Cough,
2. fever,
3. Shortness of breath.
Physical exam:
1. Tachypnea,
2. Central cyanosis,
3. Increase in tectile fremitus,
4. Dullness to percussion,
5. Reduced breath sounds,
6. rales,
7. Bronchial breathing.
Labs:
1. FHG,
2. Basic metabolic panel,
3. Sputum and blood cultures,
4. Pulse oximetry,
5. ABGs,
Imaging:
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1. CXR infiltration or consolidation.,

2. CT chest.
Management:
1. Antibiotics,
2. Rest,
3. Analgesics
4. IV fluids.

68. Perforated duodenal ulcer how to diagnose

signs and symptoms:
1) typical symptoms of perforation include :
2) sudden onset of severe abdominal pain,
3) radiation of pain to the shoulder,
4) nausea and vomiting.
signs are :
1. rigid board like abdomen
2. shock.
3. Erect CXR and look for air under the diaphragm.
Rx.
1) Simple operative closure of the perforated ulcer,
2) Definitive treatment of the ulcer e.g by vagotomy or antrectomy)

69.How to diagnose abdominal penetrating/ blunt injury

Blunt- Pt Stable or Unstable.
In stable pts Do:
a)FAST,focused abdominal sonography for trauma
Four views:
i. Morrisons pouch(RUQ):free fluid can be visualized between the liver and kidney
ii. Splenorenal recess(LUQ) free fluids can be visualized between the spleen and the kidney
iii. Pouch of douglas lie above the rectum
iv. Subxiphoid and parasternal views to look for hemopericardium
b) DPL (Diagnostic peritonaeal lavage,Open and closed )
i. Infra umbilical, direct 2 way catheter to the pelvis and aspirate.
ii. Blood > 10ml or bowel content asperated, test is +ve.
iii. Put NS half a liter and drain it, check WBC, RBC, amylase, lipase, bilirubin, bacteria.
c) CXR for air under the diaphragm,
d) CT Abdomen.
If pt unstable:
1. Resuscitate, Gain iv access 2 large bore,
2. Give 2 liters of crystalloids,
3. GXM, FHG, UECs,
4. ABG analysis,
5. Do FAST, take pt to the ER.
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Penetrating:
1. know the cause, how long,
2. Hemodynamic situation.
3. Surgery is indicate in gunshot wound,
4. Blast injury,
5. Stab wound with evisarisation,
6. Brisk bleeding,
7. Low BP with tachycardia.

70. How to manage cerebral edema

General measures:
1. Optimal head and neck positioning for facilitation of intracranial venous outflow,
2. Avoidance of dehydration and systemic hypotension,
3. Maintainance of normothermia.
Specific therapeutic interventions:
1. controlled hyperventilation,
2. administration of corticosteroids or diuretics,
3. Osmotherapy,
4. pharmacological cerebral metabolic suppression.
NB primary goal of these measures is to optimize cerebral perfusions, oxygenation and venous
drainage)

71.Hemorrhoids grading and management

vascular and connective tissue cushions in anal mucosa.
3 main cushions:
1. Left lateral,
2. Right posterior
3. Right anterior areas of the anal canal.
Classification:
Internal hemorrhoids :found superior to the dentate line with columnar epithelium, have autonomic
inervation thus not painful,
1) 1º no prolapse,
2) 2º spontaneous prolapse with spontaneous reduction,
3) 3º prolapse with manual reduction,
4) 4º permanent prolapse.
External hemorrhoid :found below the dentate line, lined by squamous epithelium, inervated by
cutaneous nerve thus painful.
Etiology:
1) constipation/straining,
2) pregnancy,
3) ascites/abdominal tumor,
4) portal hypertation.
Ddx.:
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1. Carcinoma of the colon and rectum,

2. diverticular disease,
3. adenomatous polyps,
4. ulcerative colitis,
5. rectal prolapse,
6. ulcer/fissure.
Management 6s,
1. Stool softeners and diet modification,; diet rich in roughage plus alot of water,
2. Suppositories and astrigents,
3. Sits baths.
4. Sclerotherapy.
5. Strangulation-band.
6. Surgery ie fuerguson, milligan-morgan procedure)

72. Prostatectomy types

Turp& open, complication (rem : Turp syndrome)
Indication of open Prostatectomy (ans: if prostate is large more than 70g)
1. Acute urinary retention
2. Persistent or recurrent urinary tract infection
3. Significant hemohage or recurrent hematuria
4. Bladder calculi secondary to bladder outlet obstruction
5. Significant symptoms bladder outlet not response to therapy
6. Renal insufficiency secondary to chronic bladder outlet obstruction
Types:
a) transuretral procedures-transurethral resection of the prostate turp,
(indicated for small prostates 50-60g,)
I. transurethral insition of the prostate-<30g,
II. transurethral laser induced prostatectomy tulip,
III. transurethral microwave thermoterapy.
b) open prostatectomy:
i. Transvesical prostatectomy/frayers,
ii. Retropubic/millins.
Complications:of TURP:
1) Hematuria/haemorrhage,
2) infection/prostatitis,
3) incontinence,
4) retrograde ejaculation,
5) erectile dysfunction,
6) hematospermia,
7) urethral stricture,
8) clot retation/near stricture,
9) Post TURP syndrome (use of 1.2% glycine) ie
a. hypervolemia,
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b. hypertension,
c. bradicardia,
d. pulmonary edema,
e. CHF,
f. hyponatemia,
g. hypoosmolarity,
h. cerebral edema,
i. headeache confusion.
j. RX:diuresis furosemide+mannitol, rapture of denonvilliers fascia causing feacal fistula,
10% recurrence within 10 yrs.)

73. Hernias types, complication, management and where they occur

Hernia is an abnormal protrusion of intraabdominal tissue through a fascial defect in the abdominal
wall.
Types:
1. Reducible,
2. Irreducible,
3. Obstructed,
4. Strangulated,
5. Sliding hernia ie contains an organ,
6. Ritchers hernia ie portion of the bowel wall becomes traped,
7. Inflamed.
Anatomical classification:
1. Inguinal,
2. umbilical,
3. femoral,
4. epigastric hernia,
5. diaphragmatic hernia,
6. ventral hernia.
Complication:
1. strangulation,
2. intestinal obstruction,
3. intestinal necrosis,
4. peritonitis,
5. recurrence,.
Management:
surgical repair:
1. The principal is tension free repair.
2. Bassini repair,
3. MCvy repair (copper ligament repair),
4. Marcy repair,
5. Lichtenshtein repair(placement of mesh over the defect, many prefer placement of the mesh
under defect to reduce recurrence),
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6. Shouldice repair,
7. Laparascopic repair eg TAPP transabdominal preperitoneal,
8. TEP-ELM totally extra peritoneal/extra peritoneal laparascopic repair,
9. IPOM intra peritoneal onlay mesh.
Indications for laparascopy:
I. recurrent hernia after repair,
II. bilateral inguinal hernias.
Contraindication for mesh placement:-
strangulated or perforated bowel found in hernia sac, this must be reseced and a tradional repair be
done.

74. Reasons why fistulas don’t close (Mneumonics HIS FRIEND)

H: high output fistula
I: intestinal destruction
S: short segment of the fistula <2cm
F:foreign body
R:radiation
I:infection
E:epithelialization
N:neoplasm
D:distal obstruction

75. Anatomy and localization of spleen

1. The spleen develops in the left of the dorsal mesogastrium during the fifth intrauterine week.
2. The odd numbers 1,3,5,7,9,11 summrize statistic features of the spleen, 1x3x5 inches, weighs 7 oz,
lies btw the 9th and the 11th ribs.
3. In order to palpate below the costal margin, the spleen has to atleast double in size.
4. The spleen is enveloped in parietal peritoneum, creating folds that form suspensory ligaments of
the spleen, the important folds are splenorenal ligament and gastrosplenic ligament, the former
extends btw anterior surface of the left kidney to the splenic helium and invests splenic vessels
and the pancreas, the later is a conduit for the short gastric artery.
5. Thesplenocolic and splenophrenic ligaments are usually short and avascular, woundering
spleen results from the absence of normal ligamentous attachment.
6. The splenic artery is one of the main branches of celiac axis, runs a secrpentine course over
the pancreas to the splenic helium, splenic vein joins the inferior mesenteric vein then superior
mesenteric vein then the portal vein.
7. Accessory spleens are tiny nodules of splenic tissue separte from the main gland commonly found
in the splenic helium.
8. Splenic parenchyma is divided by trabeculae which carries branches of the splenic vessels in the
parenchyma, red and white pulps are separeted by the marginal zone.
9. Spleen is prone to torsion, splenopexy is indicated.

76.Complication of blood transfusion

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1) acute hemolytic transfusion reaction ie ABO incompatibility.

2) delayed hemolytic transfusion reaction.
3) febrile nonhemolytic transfusion reaction; lasts a few hours due to Ag reaction against WBC.
4) allergic reaction to plasma.
5) transfusion related acute lung injury ARDS Ab against granulocytes.
6) volume overload.
7) altered O2 affinity.
8) graft vs host disease.
9) dilutional coagulopathy ie ascidosis, hypothermia, bleeding.
10) infections
11) iron overload
12) hypoglycemia-citrate in preserved blood binds with ca.
13) hyperkalemia

77.Cerebral vascular accident

sudden onset of neurological deficits that is as a result of cerebral vascular disease.
TIA- focal neurological deficit the lasts <24hrs caused by temporary imparement vascular suply to
brain ie emboli, aortic stenosis, vascular spasm.
Risk factors are;
1) HTN,
2) DM,
3) CAD,
4) tobacco,
5) hyperlipidemia,
6) hypercoagulable states.
H/P:
a) sudden appearance of focal neurological deficits eg weakness, parasthesias, brief unilateral
blindnessie amaurosis fugax, or other vision abnormalities, impared coordination, vertigo.
b) carotid bruit suggests carotid atherosclerosis.
c) harsh systolic murmur suggest carotid atherosclerosis.
DX:
1. US to quantify degree of carotid or aortic stenosis,
2. MRI or CT demonstrate areas of brain ischemia,
3. MRA or CT angiography locate intracranial vascular defect,
4. echocardiography to check for septic emboli, mural thrombus or patent foramen ovale.
Rx:
1. If disease atributed to atherosclerosis, give antiplatelets and statins.
2. Carotid endarterectomy or angioplasty is performed for carotid narrowing.
3. B blockers, valvuloplasty or valve replacement in aortic stenosis.
4. Long term anticoagulation used for arrhythmias.
5. Treat underlying disorder.

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Stroke-Acute Focal neurological deficit lasting> 24hrs caused by ischemia of brain via impaired
perfusion ie ischemic stroke, or hemorrhage ie hemorrhagic stroke. Ischemic stroke may be
thrombotic or embolitic.
Risk factors:
1) Increased age,
2) Family hx,
3) Obesity,
4) DM,
5) HTN,
6) Tobacco use,
7) A fib.
H/P:
a)sudden appearance of focal neurological deficits lasting > 24hrs,
b) symptoms depend on location of pathology;
ACA-
I. contralateral lower extremity
II. trunk weakness.
MCA-
i. contralateral face and upper extremity weakness and decreased sensation,
ii. bilateral visual abnormalities,
iii. aphasia ie if dominant hemisphere,
iv. neglect,
v. inability to perform learned actions ie if non dominant hemisphere.
PCA-
I. contralateral visual abnormalities,
II. blindness if bilateral PCA involvement.
Lacunar arteries-
i. focal motor and sensory deficits,
ii. loss of coordination,
iii. difficulty speaking.
Basilar artery-
I. cranial nerve abnormalities,
II. contralateral full body weakness and decreased sensation,
III. vertigo, loss of coordination,
IV. difficulty speaking,
V. visual abnormalities and coma.
c) stable finding indicates stable stroke but progressive findings indicate evolving stroke,
d) thorough neurovascular exam done to determine region of involvement.
Diagnosis;
1. Head CT without a contrast to differentiate ischemic from hemorrhagic,
2. MRI to evaluate for subacute infarction or hemorrhage,
3. MRA,
4. CTA,
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5. ECG to rule out new onset arrhythmias,

6. Carotid doppler ultrasound to rule out carotid stenosis,
7. Echocardiogram to rule out embolic sources.
Rx.:
1. Do CT scan,if hemorrhage is ruled out and no contraindications eg recent surgery, anticoagulant
use, recent hemorrhage, BP > 185/110mmhg, within 3 hrs give asprin, if it fails give plavix.
2. Other antiplatelets are clopidogrel, ticlopidine, aggrenox.
3. LMWH should be considered in pts having thromboembolism and worsening symptoms.
4. Statins and antihypertensive drugs should be started after the acute stage of stroke, NB do not
treat HTN immediately following stroke unless extreme > 220/120 or pt has CAD to maintain
cerebral perfusion.
Acute treatment of hemorrhagic stroke:
1) reversal of anticoagulation, control of BP and ICP ie mannitol, hyperventilation, anesthesia.
2) Surgical decompression. Antiplatetlets started 2 weeks after stroke in stable pts.
3) Physical therapy and treatment of underlying disorder.

78.Anemia
a. This is a decrease in RBC mass,
b. Hemoglobin,Hematocrit,
c. In Kenya hemoglobin <10g/dl
d. WHO Hb <12g/dl is defined as anemia.
Classification by mean corpuscular volume MVA:
I. Microcytic, MCV <80 (iron deficiency, lead poisoning, chronic diseases, sideroblastic and
thalasemia).
II. Normocytic MCV 80-100 ( hemolytic, chronic disease and hypovolemic).
III. Macrocytic MCV > 100 ( Folate deficiency, vit B12 deficiency, liver diseases).

A. Iron deficiency anemia: insufficient heme production secondary to insufficient iron supplies.
Causes:
I. Iron loss exceeds intake.
II. blood loss,
III. poor dietry intake or absorption,
IV. pregnancy or menstruation.
H/P:
I. fatigue,
II. weakness,
III. dyspnoe on exertion,
IV. pica ie craving ice, dirt etc,
V. pallor,
VI. tachycardia,
VII. tachypnoe,
VIII. increased pulse pressure,
IX. possible systolic murmur,
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X. angular cheilitis ie irritation of lips and corners of mouth,

XI. glossitis,
XII. spooning of nails ie koilonychia in sever cases.
Labs:
i. decreased Hb, Hct, MCV, reticulocyte, ferratin, iron,
ii. increased transferrin ie total iron binding capacity,
iii. positive stool guaiac test if secondary to GI bleeding.
iv. Blood smear- hypochromic, microcyticRBC with low reticulocyte count.
Rx.
i. Iron supplimentation for 4-6 months,
ii. oral iron sulfatedextran oriv iron dextran,
iii. determine cause of iron loss.

B. Hemolytic anemia: RBC life span shortened and bone marrow not able to meet demand for new
cells. Mean RBC life span =120 days.
caused by either:
1. membranopathy,
2. enzymopathy,
3. Hemoglobulinopathy or
4. extracellular effect.
H/P;
1) possibly asymptomatic, 10) jaundice,
2) weakness, 11) palpitation,
3) fatigue, 12) syncope,
4) dyspnoe on exertion, 13) mental status change,
5) pallor, 14) angina,
6) tachycardia, 15) chills,
7) tachypnoe, 16) abdominal pain,
8) increased pulse pressure, 17) hepatosplenomegally,
9) passible systolic murmur, 18) brownish discolouration of urine.

Labs:
1) Decreased Hb, Hct, serum heptoglobin,
2) Increased reticulocyte count,indirect bilirubin, LDH,
3) Normal MCV,
4) coombs test: reagent is rabbit IgM directed against human IgG and compliment.
5) Direct test; reagent mixed with RBCs, agglutination indicates presence of IgG and compliment on
RBCs membrane eg warm and cold agglutinin disease.
6) Indirect test: patients serum mixed with type O RBCs which in turn are mixed with coomb
reagent, agglutination indicates presence of anti RBCs antibodies in serum eg Rh
alloimmunization.
Types:
1) drug induced,
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2) autoimmune RBCc destruction,

3) mechanical RBC destruction,
4) hereditary spherocytosis,
5) G6PD deficiency.

C. Lead poisoning anemia;

a. Inhibition of heme synthesis by lead ingestion.
b. Similar anemia in alcoholism and isoniazide use.
H/P:
1. fatigue,
2. weakness,
3. abdominal pain,
4. arthralgias,
5. headache,
6. Impaired short term memory,
7. pallor mental developmental delay,
8. gingivial lead lines,
9. peripheral neuropathy.
Labs:
a. Decreased Hb, Hct, MCV,
b. increased serum lead.
c. Blood smear; microcytic RBCs, basophilic strippling of RBCs, ringed sideroblastsin the bone
marrow.
Rx.
 Remove source of lead EDTA or dimercaptosuccinic acid if needed for lead chelation, add
dimercaprol in children.

D. Folate deficiency anemia:

Causes:
a. Inadequate folate intake,
b. Increased folate need eg poor nutrition, chemotherapy,
c. Drug induced folate metabolism defect eg methotraxate, trimethoprim, phenytoin.
H/P:
1. poor nutrition,
2. fatigue,
3. weakness,
4. dyspnoe,
5. increased pulse pressure,
6. possible systolic murmur,
7. no neurological symptoms.
Labs:
I. Decreased Hb, Hct, serum folate, red cell folate level, reticulocyte count,
II. increased MCV.
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III. Blood smear; macrocytic RBCs, hypersegmented neutrophils.

Rx. Oral folate supplementation.

E. Vit B12 deficiency anemia:

Causes:
1. Pernicious anemia ie autoimmune anemia owing to lack of intrinsic factor, or
2. anemia resulting from inadequate vitamin B12 intake,
3. ileal resection,
4. bacterial overgrowth in GI tract, or
5. warm infestation.
H/P:
a. fatigue,
b. weakness,
c. dyspnoe on exertion,
d. memory loss,
e. tachycardia,
f. tachypnoe,
g. increased pulse pressure,
h. possible systolic murmur,
i. symetric parasthesia,
j. ataxia,
k. possible psychosis.
Labs:
a) Decreased Hb, Hct, vit B12,
b) Increased MCV,
c) Schilling test: administer oral radioactive lebeled vit B12, normal lebeled vit B12 exctetion(etiology
other than perniciuos anemia) if decreasd labeled vit B12 excretion, repeat test with addition of
intrinsic factor, normal labeled vit B12 excretion (pernicious anemia), decreased labeled vit B12
excretion(intestinal malabsorption).
d) Blood smear macrocytic RBCs hypersegmented neutrophils.
Rx.
1. Monthly intramascular vit B12 injuction,
2. Dietry supplimentation
3. Intranasal vit B12.

F. Anemia of chronic diseases:

Causes:
a) In pts with neoplasia,
b) DM,
c) Autoimmune disorders,
d) Long standing infections.
e) Frequently associated with trapping of iron in macrophages,
f) Decreased erythropoetin production,
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g) Increased hepticidin levels ie inhibitor of iron absorption and mobilization.

H/P:
a) Hx of appropriate disease state,
b) fatigue, weakness,
c) dyspnoe on exertion,
d) tachycardia,
e) pallor.
Labs:
1. mildly decreased Hb, Hct, normal or decreased MCV,
2. decreased iron, transferrin,
3. normal or increased ferratin.
4. Blood smear: normocytic RBCs.
Rx. Treat underlying disorder, supplimental erythropoetin.

G. Anaplastic anemia:
pancytopenia resulting from bone marrow failure.
Causes:
1. drugs eg chloramphenicol, sulfonimides, phenytoin,
2. chemotherapies,
3. toxins,
4. radiation,
5. viral infection,
6. idiopathic and congental causes.
H/P:
1. fatigue, weakness,
2. persistent infections,
3. poor clotting with possible uncontrolled bleeding,
4. easy bruising,
5. persistent menstration,
6. pallor, petechiae,
7. tachycardia, tachypnoe,
8. increased pulse pressure,
9. systolic murmur.
Labs:
1. Decreased Hb, Hct, WBC, platelets,
2. hypocellularity and fatty infiltrates of bone marrow.
Rx.
a) Stop offending agent,
b) transfuse for acute anemia and thrombocytopenia,
c) bone marrow transplant.

79.SLE

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multisystem autoimmune disorder involving a variety of autoantibodies affecting several body

systems. Antibody mediated cellular attack occurs with deposition of antigen antibody complexes in
affected tissues.
Risk factors: young women, blacks, asians, hispanic.
NB: hydralazine, procainamide, isoniazide methyldopa, quinidine and chlorpromazine can cause
similar symptoms that resolve when the drug is discontinued.
H/P: non specific symptoms eg fever, anorexia, weight loss and symettic joint pain.
Criteria for diagnosis mnemonic DOPAMINE RASH, pt with 4 of the ctiteria is likely to have SLE 96%
sensitivity.
1. Discoid rash.
2. Oral ulcer.
3. Photosensitivity.
4. Arthritisie systemic nonerrosivearthritis in PIPs, MCPs, wrist, knee and feet.
5. Malar rash.
6. Immunologic criteriaie anti double stranded DNA antibodies, anti smith antibodies,
antiphospholipid antibodies.
7. Neurologic symptoms eg lupus cerebritis, seizures, stroke, psychosis, neuropathy.
8. Elevated ESR.
9. Renal diseaseie immune complex glomerulnephritis, interstitial nephritis, proteinuria, increased
BUN and creatinin.
10. ANA positive.
11. Serositis ie pleuritis, pericarditis, pneumonitis.
12. Hematologic abnormalitiesie autoimmune hemolytic anemia, leukopenia, thrombocytopenia.
Dx.
1) +ANA is highly sensitive but not specific.
2) Anti dsDNA and anti-Sm antibodies are highly specific but not as sensitive.
3) In drug induced SLE + antihistone antibodies.
4) Neonatal SLE is associated with +anti Ro antibodies transmitted from mother to neonate.
5) Also can find antiphospholipid antibodies, decreased compliment C3 and C4, anemia, leukopenia
and thrombocytopenia, proteinuria and casts.
Rx.
1. Avoid dirrect sunlight,
2. NSAIDs for mild joint symptoms,
3. Corticosteroids for acute exercerbations.
4. Corticostetoids, hydoxychloroquine, cyclophosphomide and azathioprine can be used for
progressive or refractory cases.
5. Hydroxychloroquine is used in isolated skin and jiont involvement.
6. Cyclophoshamide is used in sever cases of lupus nephritis.
Complications:
1) Lupus anticoagulant and anticardiolipin antibodies increase the risk of miscarrage and fetal death.
Some cases remain benign and others progress rapidly.
2) Pts death occurs as aresult of lung, heart, brain and kidney function impairment.

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3) NB: libman sacks endocarditis is non infectious vegetation seen on mitral valve in association with
SLE and antiphospholipid syndrome. SLE can cause a +VDRL test.

80.Curb-65 ( pneumonia severity score:

C: Confusion, GCS (1 point.)
U: Urea, BUN> 19 (1 point.)
R: Respiratory rate > 30 (1 point.)
B: BP <90/60 (1point.)
65: Age> 65 (1 point.)
0-1 point low risk.
2-5 points high risk.

81.Toxoplasmosis
Toxoplasma gondii.
Risk factor:
 ingestation of raw or uncooked meat, and changing cat litter.
H/E:
1. Primary infection is usually asymptomatic.
2. Reactivated toxoplasmosis occurs in immunosuppressed patients and may present in specific
organs ie brain, lung, eye, heart, skin, GI tract and liver.
3. Encephalitis is common in seropositive AIDS pts.
4. Classically CNS lessions present with fever, altered mental status, seizures and focal neurologic
deficits.
Dx.
1) Serology, PCR (indicates exposure and risk for reactivation),
2) tissue examination for histology,
3) isolation of the organism in mice, or tissue culture.
4) In the setting for CNS involvement, obtain a CT scan look for multiple isodense or hypodense ring
enhancing mass lesions, or
5) MRI has predilection for the basal ganglia, more sensitive.
Rx.:
1. Induction with high dose PO pyrimethamine + sulfadiazine and leucovorin (folic acid analog to
prevent hematologic toxicity) 4-8 weeks,
Maintainance with a low dose untill the disease has resolved clinically and radiologically.
2. TMP-SMX (bactrim DS) or pyrimethamine + dapsone can be used for prophylaxis in pts with
CD4+ count <100mm^3 and a + toxoplasmosis IgG.
Effect on the fetus/neonate:
1) hydrocephalus,
2) intracranial calcifications,
3) chorioretinitis,
4) microcephaly,
5) spontaneous abortion,
6) seizures.
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Dx. Possible mononucleosis like illness, amniotic fluid PCR for toxoplasma gondii, or serum antibody
screening.)

82.New York heart association classification of heart failure

1) Class I no limitations.
2) Class II slight limitation.
3) Class III marked limitations
4) Class IV symptomatic at rest.

83. CRAG (cryptococcal antigen test)

1. Highly sensitive and specific test for cryptococcal meningitis compared to traditional methods of
microscopy (india ink staining) and culture.
2. Lateral flow assay dipstick is used.
3. Serum specimen: sensitivity of 100% and specificity of 99.5%.
4. CSF specimen: sensitivity of 100% and specificity of 97.7%.)

84. Vacuum dressing

Negative pressure wound therapy provides an occlusive controlled sub-atmospheric
pressure(negative pressure) suction dressing that promotes moist wound healing.
1) It improves tissue perfusion,
2) stimulate granulation tissue,
3) reduces edema and excessive wound fluid,
4) reduces overall wound size.
Indications:
1. pressure ulcers,
2. venous ulcers,
3. diabetic foot ulcers,
4. dehisced surgical incisions,
5. pertial thick ness burns,
6. Skin grafts,
7. split thickness skin graft,
8. traumatic wounds,
9. fasciotomy, myocutaneous flaps,
10. temporary closure for abdominal compartment syndrome.
Contraindications:
1) exposed arteries or veins,
2) malignancy in the wound bed,
3) active bleeding or coagulopathic pts,
4) untreated osteomyelitis,
5) nonenteric unexplored fistulas,
6) necrotic tissue with eschar present,
7) sensitivity to silver.

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85. RHD, endocarditis, ventricular heart disease, heart failure

Acute rheumatic fever:
uncommon sequela of untreated group A streptococcus infection.
Provokes antibodies that attack joints and the heart valves(mitral> aortic> tricuspid).
H/P:
Johns criteria: menemonics:
1. Major criteria-
CASES (Carditis, Arthritis, Sydenham chorea,Erythema marginatum and Subcutaneous nodules),
2. Minor criteria-
PEACE (Previous rheumatic fever, ECG with PR prolongation, Arthralgias, CRP and ESR elevated and
Elevated temperature).
Diagnosis of RHD:
1) Hx of recent streptococcal infection and either the presence of
2) 2 major criteria or 1 major with 2 minor criteria.
Labs:
1. increased ESR, CRP, WBC, antistreptocaccal antibodies.
2. ECG increased PR interval.
Rx.
1. NSAIDs for joint inflammation,
2. Corticosteroids,
3. Penicillin beta lactam for infection.

Valvular heart diseases:

1. Aortic stenosis-
causes: congenital defect, RHD, calcifications in elderly, tertiary syphilis.
Symptoms:
I. chest pain,
II. dyspnoe on exertion,
III. syncope.
Exam:
i. weak prolonged pulse,
ii. cresendo-decresendo systolic murmur radiating to carotids,
iii. weak S2,
iv. valsalva decreases murmur.
Radiology: calcified aortic valve, dilated aorta on CXR, echo and cardiac cathererization helpfull in
diagnosis.
Rx. Valve replacement.

2. Mitral regurgitation-
Causes: mitral valve prolapse, RHD, papilary muscle dysfunction, endocarditis, LV dilation.
Symptoms:
i. Asymptomatic in mild cases,
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ii. Palpitations,
iii. Dyspnoe on exertion,
iv. Orthopnoe,
v. PND.
Exam:
I. Harsh blowing holosystolic
II. Murmur radiating from apex to axilla,
III. S3, widely split S2,
IV. Midsystolic click.
Radiology: LVH and LA enlargement on CXR, echo helpful for diagnosis.
Rx.
i. Vasodilators if symptomatic,
ii. prophylactic antibiotics for increased infection risk,
iii. prophylactic anticoagulation,
iv. surgical repair in severe or acute cases.

3. Aortic regurgitation-
Causes: congenital defect, endocarditis, RHD, tertiary syphilis, aortic root dilation from aortic
dissection.
Symptoms:
I. initially asymptomatic,
II. dyspnoe on exertion,
III. chest pain,
IV. orthopnoe.
Exam:
i. bounding pulse,
ii. widened pulse pressure,
iii. diastolic decresendo murmur at right second ICS,
iv. late diastolic rumble ie austin-flint murmur,
v. cappilary pulsations in nail bed ie quincke sign.
Radiology: dilated aorta and LV enlargement on CXR, echo helpfull in diagnosis.
Rx.
i. ACE inhibitors,
ii. calcium channel blockers or nitrates (decreases afterload),
iii. valve replacement.

4. Mitral stenosis-
causes: RHD.
Symptoms: initially asymptomatic(almost 10 yrs), dyspnoe on exertion, orthopnoe, PND, peripheral
edema, hepatomegaly.
Exam: opening snap after S2, diastolic rumble, loud S1.
Radiology: RVH, LA enlargement, and mitral valve calcification on CXR, echo helpfull for diagnosis.
Rx.
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i. Diuretics (reduce preload),

ii. Antiarrhythmics for Afib secondary to atrial enlargement,
iii. Surgical repair prior to symptomatic progression.

Infective Endocarditis:
bacterial infection of endocardium +/- valve involvement.
Common in pts with congenital heart defects,
intravenous drug abuse or prosthetic valves.
Pts with SLE may present with non infective endocarditis ie libman-sacks endocarditis.
Forms: acute and subacute.
Acute endocarditis is caused by staph aureus, strep pneumonae, strep pyogens, neisseria
gonorrhoeae. Sub acute is caused byviridans streptococci, enterococcus, fungi and staphylococcus
epidermidis.
Dx.
Use dukes criteria- definitive diagnosis of infective endocarditis requires
1. Direct histologic evedence of IE,
2. Positive gram stain from surgical debridement of cardiac abscess or autopsy specimen,
3. 2 major criteria, OR 1 major and 3 minor criteria, OR 5 minor criteria.
Major criteria
a. Serial blood cultures positive for organisms associated with IE,
b. Presence of vegetations or cardiac abscess seen on echocardiogram,
c. Evidence of new onset valvular regurgitation,
d. Blood cultures positive for Coxiella burnetii).
Minor criteria
a. Predesposing heart condition or IV drug use,
b. Fever > 38ºc,
c. Vascular phenomenoneg arterial emboli, septic pulmonary infarct, mycotic aneurism, intracranial
hemorrhage, conjuctival hemorrhage and janeway lesions,
d. Immunologic phenomenon ie glomerulonephritis, osler nodes, roth spots and positive RF,
e. Positive factors not meeting requirements of major criteria, or serologic evidence of infection
without positive culture.
H/P:
i. fever, chills, night sweats, fatigue,
ii. arthralgias,
iii. possible new murmur,
iv. Osler nodes, janeway lesions, splinter hemorrhage, roth spot.
Labs:
a. Serial blood cultures,
b. Increased CRP, ESR.
Radiology:
a) Echocardiogram shows vegetations on valves,
b) CXR may show right sided heart failure.
Rx.
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i. Long term ie 4-6 weeks of antibiotics,

ii. antibiotics prophylaxis before surgery, dental work.
iii. Valve replacement for severly damaged valves.
iv. NB: negative culture endocarfits can result from HACEK bacteria (haemophilus, actinobacillus,
cardiobacterium, ekenellaand kingella).

86.TURP -Transurethral resection of the prostate

BPH-benign adenomatous hyperplasia of the periurethral prostate gland causing bladder outlet
obstruction.
H/P:
i. Urinary hesitancy,
ii. Straining,
iii. Weak/intermittent stream,
iv. Dribbling, f
v. Requency, urgency,
vi. Nocturia,
vii. Urge incontinence develops secondary to incomplete empting or UTI,
viii. DRE-normal anal sphincter tone, prostate is firm, smooth and mucus over is mobile, medial
sulcus felt and symmetry maintained.
Labs: mild increase in PSA, urinalysis, biopsy and renal gunction tests.
Radiology: transrectal US shows enlarged prostate.
Rx.
i. Alpha 1 redeptor blockers eg terazosin,
ii. 5 alpha reductase inhibiors eg finasteride,
iii. TURP, tranurethral needle ablation.
iv. TURP- transurethral resection of the prostate.
v. Standard procedure with low morbidity.
Complications :
1. Include bleeding, failure to void, infection and TURP syndrome ie severe hyponatremia due to
absorption of hypotonic solution used intraoperatively.
2. Symptoms are referable to exess ammonia production ie glycine metabolite, exess fluid
absorption ie hyponatremia, hypervolemia or both ie water intoxication.
3. Irrigation: D5, mannitol, glycine, furisol, plain water. NB: RL and NS cannot be used coz they
contain electrolytes that conduct electricity away from operating site.
4. Manifestations of TURP syndrome: hypervolemia, hypertention, bradicardia, pulmonary edema,
CHF, hyponatremia, hyperosmolarity, cerebral edema, headeache, confussion.
Rx.Diuresis+furosemide+mannitol.

87.DKA- DM
Extreme low insulin and exess glucagon causes degeneration of triglycerides into fatty acids and
eventual conversion into ketoacids.
Causes:
i. Mostly in pt with type 1DM,
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ii. Who do not take prescribed insulin, or have infections,

iii. High stress,
iv. MI,
v. High alcohol use or surgery.
H/P:
i. Weakness, polyuria, polydipsia,
ii. Abdominal pain, vomiting, dry mucus membranes,
iii. Decreased skin turgor,
iv. Fruity odour on breath,
v. Hyperventilation ie kussmaul respiration=deep,
vi. Laboured and regular breathing,
vii. Mental status changes develop with worsening dehydration.
Labs:
i. hyperglycemia ie 15-50mmole/l,
ii. decreased Na+,
iii. normal or increased serum K+,
iv. decreased phosphate,
v. high anion gap metabolic acidosis,
vi. serum and urine ketones.
Rx.(FIKAP)
1. IV Fluids,
2. Insulin,
3. KCl,
4. Tx Anion gap
5. Prevention of underlying infection.
6. Success in treatment may be confirmed by closure of the anion gap.

88.Description of abdominal plain film, CT

(AXR: Indications-
i. suspected bowel obstruction,
ii. foreign body,
iii. stones in the renal tract,
iv. to check for position of stent.
Procedures
i. Date of the x ray taken.
ii. Name age and sex.
iii. Projection, Orientation, Penetration, Adequacy.
iv. Bowel. Gas-amount, distribution, extraluminal. Soft tissue-psoas,spleen, liver GB, KUB.Bones-spine
and pelvis.
v. Any calcification. Aorta-cacified? Widened? Any other structures-iatrogenic, accidental,
projectional.

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Projection- usually AP. Supine- unless otherwise lebeled otherwise, the film will probably be supine.
Erect-usefull in looking for fluid levels. Decubitus-to detect intraperitoneal gas. Prone-pt lying on the
their front, used in IVU.
Orientation; pelvic bones at the bottom, ribs angle downwards and outwards, liver opacity on the left
of the screen ie pts right.
Adequecy: is the whole abdomen representedie xiphisternum to the symphisus pubis.
Penetration: can you see spinous processes through the vertebral bodies.
Small and large bowel: small bowel-<3cm in diameter, in the center, many loops, has vulvulae
conniventes.
Large bowel: <5cmin dameter, in the periphery, few loops, has haustra.OR(demographics ie this is an
abdominal radioghraph of mr X, in supine AP position, taken on 21/12/2112.
Then PFR:
Penetration-exposure, under exposure, good and over exposure.
Field: diaphram to the groin.
Rotation.
Most obvous abnormality e.g
i. Pneumoperitoneum i.e subphrenic air,
ii. SBO-distended bowel,
iii. Airfluid levels,
iv. LBO-distended large bowels,
v. Sigmoid volvulous-coffee bean sign,
vi. Sentile loop-isolated ileus due to adjacent inflamation.
vii. RUQ-cholecystitis,
viii. RLQ-appendicires,
ix. LUQ- pancreatitis,
x. LLQ- diverticulitis.
Systematic: ABC:
A- Air, intraluminal-small bowels no air. Intramural- ischaemic colitis. Extraluminal-billiary treeie
gallstone ileus,diaghram in erect view.
B- Bone and calcification- normal calcification spine, aorta. Abnormal calcification gallstone, pancreas,
urinary tree stone.
C-Spleen, psoas shadow, absence indicates intra abdminal or retroperotoneal fluid, eg rapture AAA,
ascites.
Summary: in summary, this is an abdominal radiograph of mr, X, in supine AP position, taken on
12/21/4325. There are signs os_______ in line with the diagnosis of _______.

89.Description of abdominal mass

1. site,
2. size,
3. shape,
4. skin,
5. surface,
6. consistency,
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7. mobility,
8. tenderness,
9. local lymph nodes.

90. HIV-AN (associated nephropathy)

Renal disease is a common complication in HIV, it can result from:
a) Direct kidney infection with HIV ie HIV-AN,
b) Opportunistic infection or neoplasm,
c) Side effects of HIV drugs eg pentamidine, Amphotericine B, tenofovir, TMP-SMX, sulphadiazine,
indinavir.
d) Prerenal azotemia.
HIV-AN:
 Due to direct infection by HIV virus.
 Pentad of findings: proteinuria, azotemia, normal BP, normal to large kidney on US, focal
segmental Glomerulosclerosis on renal biopsy.
 HIV AN has both tubulointestinal and glomerular components.
Clinical presentation:
1) Nephrotic like syndrome ie a) proteinuria> 3.5 g/d, b) azotemia, c) hypoalbuminemia, also edema
and hyperlipidemia,
2) CD4 count <200cells/ml,
3) Not hypertensive even in renal insuficiency,
4) Normal to large and highly echogenic on US,
5) Urinalysis- microhematuria, leucocyturia, hyaline casts, oval fat bodies but no cellular casts,
6) Serum compliment levels are normal.
Indications of biopsy:
i. To distinguish HIV AN from other forms of renal disease eg immune complex glomerulonephritis,
IgG nephropathy.
ii. Obtain a renal biopsy if pt's daily protein excretion is > 1grm.
Rx:
i. Put pt on ARVs to retard progression to Chronic renal failure.
ii. Corticosteroids-prednisone, ACE inhibitor- captopril improves renal survival, use in pts with no
hyperkalemia and createnin level <2mg/dl.
iii. Cyclosporine in pediatric pts. Dialysis-ESRD.

91. Kaposi sarcoma

multifocal angiosarcoma.
Epidemiological classification:
a) epidemic AIDS-related KS- most common KS, it is an AIDS defining illness.
b) immunocompromised KS- following solid organ transplant, occurs 30 months after a transplant,
visceral involvement is common.
c) classic KS- occurs in elderly men of mediterenian and eastern european background, takes a
protracted and indolent course, common complication is venous stasis and lymphedema, visceral
involvement is uncommon.
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d) endemic african KS- occurs in HIV seronegative africans, may take indolent or aggressive course.
Causes:
coinfection of HIV and HHV-8, iatrogenic immunosuppression etc.
Clinical presentation:
Mucocutaneous lesions: multiple skin lesions, tumor associated lymphedema, lymphadenopathy, pain,
kobner phenomenon appears evident with nodules at site of trauma.
GI: lesions can occur anywhere within GI tract, often asymptomatic and clinically indolent,
odynophagia, dysphagia, nausea, vomiting, abdominal pain, hematemesis, hematochezia, melena,
bowel obstruction.
Pulmonary: cough, dyspnoe, hemoptysis, chest pain, asymptomatic radiographic findings.
O/E: described in 3 forms:
a) localized nodular,
b) locally agressive,
c) generalized KS.
Cutaneous KS may be exophyticor infiltrative, and occur in 6 stages:
macular (descrete red or purple patches),
papular,
plaque,
nodular (spongy to the touch),
Ulcerative,
lymphadenopathic.
Occur on the lower extremities, head and neck region.
Lesions are usually non pruritic and vary in size.
Lesions appear brown, pink, red or violaceous in colour.
Lesion may be discrete or confluent and typically appear in a linear, symmetric disribution following
langer lines.
Mucus involvements are common eg palate, gingiva, conjuctiva.
Dx.
Labs:
CD4 count and HIV viral load, FHG and ESR-anemia if hematemesis or chroni illness, UECs and LFTs-
visceral KS, before chemotherapy.
Imaging studies: CXR-diffuse reticular infiltrates, interstitial infiltrates, pleural effusions, hilar and
mediastinal lymphadenopathy, isolated pulmonary nodule. CT chest or abdomen, Abdominal US, if
limb involvement do xray-shows bone infiltrate. Thallium or gallium scans- to differentiate pulmonary
KS and infection. KS-intense thallium uptake and no gallium uptake. Definitive diagnosis: punch
biopsy, bronchoscopy, EGD, colonoscopy.
Histological types: mixed, monomorphic and anaplastic forms.
Staging:
Stage I: localized nodular KS, with> 15 cutaneous lesions or involvement restricted to one bilateral
anatomical site and few gut nodules.
Stage II: includes both exophytic destructive lesions and locally infiltrative cutaneous lesions as locally
aggressive KS.

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Stage III: generalized lymphadenopathic KS, widespread lymphnode involvement,+/- skin lesions but
no visceral involvement.
Stage IV: disseminated visceral KS, involvement of multiple visceral organs.
With each stage:
A- associated oportunistic infection is evident,
B-pt is HIV seropositive,
C- cutaneous anergy or other evidence of severe immunodeficiency is present.
AIDS clinical trial group(ACTG) staging:
Good risk:
i. Tumor T- confined to skin and lymphnodes,
ii. minimal oral disease.
iii. Imune system
iv. I- CD4 > 200 cells/ml.
v. Systemic illness S- no Hx of OI,
vi. Weight loss or diarrhea.
vii. Karnofsky performance > 70.
Poor risk:
I. T- edema and ulceration,
II. extensive oral,
III. GI KS,.
IV. I- CD4 <200cells/ml.
V. S- Hx of OI,
VI. Fever, night sweat,
VII. weight loss,
VIII. Other HIV related illness.
IX. Karnofsky performance status <70.
Rx. :
A. ARVs.
B. Local therapy: radiation therapy, intralesional vinblastine, cryotherapy, topical retinoids.
C. Systemic therapy: indicated for extensive or symptom aticvisceral disease, rapidly progressive
mucocutaneous disease and symptomatic lymphedema.
i) interferon-alfa,
ii) chemotherapy: ABVD-adriamysin, bleomycin, vincristine, dacarbazine. VAP- vincristine, adramycin,
paclitaxel.
D. Surgical care: solitary KS, acute presentation causing abdominal obstruction, perforation of
intestines, hemorrhage may be surgically excised.

92. DVT scoring system (Wells' Criteria)

1) Paralysis, paresis or recent orthopedic casting of lower extremity (1 point).
2) Recently bedridden more than 3 days or Major surgery within past 4 weeks (1 point).
3) Localized tenderness in deep vein system (1 point).
4) Swelling of entire leg (1 point).
5) Calf swelling 3 cm greater in the symptomatic leg (1 point).
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6) Pitting edema greater in the symptomatic leg (1 point).

7) Collateral non varicose superficial veins (1 point).
8) Active ca or ca treated within 6 months (1 point).
9) Alternative dx more likely than DVT e.g
i. bakers cyst,
ii. cellulitis,
iii. muscle damage,
iv. superficial venous thrombosis,
v. post phlebitic syndrome,
vi. inguinal lymphadenopathy,
vii. external venous compression (-2 points).

93. Indanavir causes

1. Gallstone (increases in cholesterol) (Causes renal calculi, present with asymptomatic hematuria
and renal colic.
2. Rx. Adequate hydration to prevent this.

94. Finger clubbing stages

Clubbing develops in five steps
1. Fluctuation and softening of the nail bed (increased ballotability)
2. Loss of the normal <165° angle (Lovibond angle) between the nailbed and the fold (cuticula)
3. Increased convexity of the nail fold
4. Thickening of the whole distal (end part of the) finger (resembling a drumstick)
5. Shiny aspect and striation of the nail and skin

95. Indication and complication of NG tube

Indications:
A) Diagnostic;
1. Evaluation of GI bleed,
2. Aspiration of gastric fluid content,
3. Identification of esophagus and stomach on CXR,
4. Administering radiographic content.
B). Therapeutic;
1. Gastric decompression,
2. Relief of symptoms in small intestine obstruction,
3. Aspiration of gastric content e.g poison,
4. Administering medication,
5. Feeding,
6. Bowel irrigation.
Complications of NG tube:
1. Discomfort,
2. Epistasis,
3. Respiratory tree intubation,
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4. Esophageal perforation.)
Types NG tubes
1. Levin
2. Dubhoff
3. Salem sam

96. Component of Bishop score

1) Dilation (cm)- 0 (closed), 1 (1-2 cm), 2 (3-4 cm), 3 (>5 cm).
2) Effacement or length- 0 (0-30%), 1 (40-50%), 2 (60-70%) 3 (>80%)
3) Station- 0 (-3), 1 (-2), 2 (-1, 0) 3 (+1,+2),
4) Consistency-0 (firm), 1 (medium), 2 (soft).
5) Position- 0 (posterior), 1 (mild), 2 (anterior).
Maximum score is 13.
> 8 good chance of viginal delivery i.e cervix is favorable.
<6 cervixis unfavorable.
In Modified bishop score add 1 point for existance of preeclampsia, and every previous vaginal
delivery. 1 point is substracted for postdate pregnancy, nulliparity and prom.)

97. Stages and management of labour

3 stages of labour.
A. 1st stage: dilation stage. Begins with onset of true labour and lasts untill cervix fully dilated to 10
cm.
B. 2nd stage: Expulsion. From cervix at 10 cm to delivery of baby.
C. 3rd stage: Delivery of placenta.
1st stage has 3 phases;
a) 1st phase is Latent phase begins with onset of labour till cervix dilated to 3 cm.
i. Duration 8-10 hours.
ii. Contractions 30-45 secs.
iii. Rest btw contractions 5-30 mins.
iv. Contractions are typically mild irregular but becomes stronger and closer together.
v. Water can break anytime during 1st phase.
b) 2nd phase is active labour phase; till cervix dilated to 7 cm.
i. Duration 3-5 hours.
ii. Contractions last 45-60 secs.
iii. Rest btw contractions 3-5 mins.
iv. Effacement of cervix is completed.
c) 3rd phase is transition phase; till cervix fully dilated to 10 cm.
i. Duration 30 min to 2 hours.
ii. Contractions 60-90 secs.
iii. Rest periods 30 sec-2 min.
iv. Contractions long strong intense and may overlap.
2nd stage of labour:
i. Expulsion, 20 min - 2 hours or longer.
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ii. Contractions 45-90 secs.

iii. Rest period 3-5 mins.
iv. Strong natural urge to push with feeling of pressure on rectum.
3rd stage:
i. Delivery of placenta. 5-30 min.
ii. Examine to be certain that all of it has been expelled.

98. Causes of per vaginal bleeding

1. Uterine fibroids,
2. Endometrial polyps,
3. Adenomyosis,
4. IUCD,
5. Hypothyroidism,
6. SLE,
7. Blood cloting disorders,
8. Pregnancy,
9. Abortion,
10. Ectopic pregnancy,
11. Placenta praevia,
12. PPH ie TTTT.

99.FIGO classification of ca cervix

Stage 0: CIN III/ carcinoma in situ.
Stage 1:Cancer confined to the cervix
Stage 1A: microinvasive carcinoma.
Stage 1B: invasive ca. Confined to the cervix.
Stage 2:Cancer extended beyond the cervix but not reached the pelvic wall
Stage 2A: tumor extending to upper 1/3 of vagina.
Stage 2B: tumor extending to the parametrium but not to the pelvic side wall.
Stage 3:Cancer has extended beyond the pelvic wall
Stage 3A: tumor involving lower 2/3 of the vagina.
Stage 3B: tumor extending to pelvic side wall, intravenous urogram reveals obstruction of ureters,
hydronephrosis.
Stage 4: Cancer extended beyond the true pelvic involve the mucosa of the bladder or rectum
Stage 4A: tumor involving the bladder or rectum.
Stage 4B: extra pelvic spread, liver, lung metastasis.)

100.Medical causes of intestinal obstruction

Small bowel obstruction:
classified by the site of the pathology relative to the intestinal wall:
a) outside the wall:
i. Adhesions,
ii. Hernia,
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iii. volvulus,
iv. Intussusception,
v. Inflammatory mases,
vi. Neoplasm,
vii. congenital bands.
b) in the wall:
i. Tumor,
ii. Tuberculosis,
iii. Congenital atresia,
iv. Crohns disease,
v. Ischemia.
c) intraluminal:
i. Gallstones,
ii. Foreign bodies,
iii. Bezoares.
Large bowel obstruction: tomor, diverticular stricture, volvulus, ischemia, crohns disease.

101.Neonatal sepsis
invasive bacterial infection occuring during neonatal period.
Etiology:
Early onset sepsis-<72hrs
Late onset sepsis-> 72hrs.
Early onset: usually results from organisms aquired intrapatum.
Most infants develop symptoms within 6 hrs after birth.
Organsims: E.coli, Acinetobacter, Klebsiella sp, GBS, Listeria monocytogens.
Late onset: usually aquired from the environment.
Organisms: group A strep, GBS, Strep pneumoniae, Staph aureus.
Risk factors-
1. males> females,
2. PROM,
3. chorioamnionitis,
4. maternal GBS colonization,
5. > 6VE during labour with PROM,
6. prematurity,
7. prolonged use of IV catheters,
8. associated illness,
9. exposure to antibiotics,
10. prolonged hospitalization,
11. Contaminated of equipments.
12. Predesposing factors- low APGAR score,
13. maternal fever> 38.3º,
14. maternal UTI,
15. poor or no ANC,
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16. poor maternal nutrition,

17. LBW, MSL,
18. difficult delivery.
Clinical presentation:
1) early symptoms are non specific eg
2) temeprature instability ie hypo/hyperthermia,
3) bradicardia, apnoe, anorexia,
4) less vigorous sucking,
5) diminished spontaneous activity.
Specific signs may pinpoint the primary/metastatic site:
1. Respiratory distress,
2. Periumbilical erythema, discharge or bleeding ie omphalitis,
3. Coma, seizures or buldging fontanelle ie meningitis,
4. Extremity swelling, warmth, erythemaie osteomyelitis or pyogenic arthritis,
5. Unexplained abdominal distention ie peritonitis or NEC,
6. Cutaneous vesicles, mouth ulcers, hepatosplenomegaly ie disseminated herpes simplex.
Dx.
1. Hx- look for predesposing factors or risk factors.
2. Physical exam- look for predesposing factors e.g LBW, skin septic spots, omphalitis etc.
3. Blood cultures-gold standard.
4. FHG.
5. CSF and Urine cultures.
6. CXR. CRP, UECs, LFTs.
Rx.
i. Antibiotics and suppotive therapy.
ii. Ensure hydration,
iii. electrolyte balance,
iv. thermal neutral environment,
v. ensure nutrition,
vi. isolate nursing,
vii. remove all indwelling catheters.
viii. Broad spectrum antibiotics parenterally before culture report. Xpen/gentamicin.
ix. Can substitute xpen for ampicillin or ceftazidine.
x. Then change antibiotics according to culture sensitivity or after 48 hrs if no improvement.
xi. Treat for additional 5-7 days after clinical response. In case of meningitis treat for 2-3 weeks.
Complications:
1. Shock,
2. Circulatory colapse,
3. DIC,
4. Severe jaundice,
5. NEC,
6. Mental retardation
7. Neurological deficits due to meningitis,
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8. Short bowel syndrome due to NEC.

102.Rickets and marasmus

Rickets is a disease characterized by bone lesions that are caused by failure of osteoid, the growing
cellular matrix of bone, to be mineralized.
The underminirelized bone is less rigid and the growing, remodeling bone bends and twists
abnormaly. Clinical features:
1) Rachitic rosary,
2) Rowing of the legs,
3) Knobby prominence of wrists and knees,
4) Growth failure,
5) Craniotabes,
6) Fractures,
7) Widening of space btw metaphysis and epyphysis,
8) Harison groove,
9) Wrist capping,
10) Richitic myopathy,
11) Knok knees,
12) Frontal boosing,
13) Kyphoscoliosis/lumber lordosis,
14) Caput quadratum.
Causes: vit D deficiency, lack of adequate Ca++ and P++.
Classification:
Causes
1. Nutritional ricket-lack of vit D in diet eg unsuplimented breast feed infants for more than 6 months,
give high dose vit D therapy,
2. Ricket accociated with abnormal metabolism of vit D-vit D dependent ricket, vit D resistant ricket ie
hereditary deficiency of vit D receptor, chronic illneses of renal or liver, chronic anticonvulsant therapy
eg phenobarbetal.
3. Rickets due to mineral deficiency: hypophosphotemic rickets, rickets of prematurity (metabolic
bone disease of the premature infant)
Rx. Vit D supplement.

103.Malnutrition management
Malnutrition- is the cellular imbalance btw supply of nutrients and energy and the body's demand to
ensure growth, maintainance and specific functions.
Classification: WHO-
-1--2 SD is mild,
-2- -3SD is moderate,
-2- -3 SD is severe.
underweight (W/A), wasting(W/H), stunting(H/A).
Wellcome trust classification-
1. Underweight: 60-80 W/A% and no edema.
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2. Kwashiorkor: 60-80W/A% and present edema.

3. Marasmus: <60W/A% and absent edema.
4. Marasmic-kwashiorkor: <60 W/A% and present edema.
5. Severe malnutrition: Dx: W/(L or H)= 70% or -3SD, bilateral pedal edema, visible severe wasting,
skin changes, hair changes.
Assesment:
Take Hx concerning:
1. Recent food and fluid intake,
2. Usual diet,
3. Breast feeding,
4. Duration and frequency of diarrhea and vomiting,
5. Type of diarrhea (watery/bloody),
6. Loss of appetite,
7. Family circumstances,
8. Chronic cough,
9. Contact with TB,
10. Recent contact with measles,
11. Known or suspected HIV infection.
O/E:
1) Look for signs of dehydration,
2) Shock(cold hands, slow capillary refill, weak and rapid pulse),
3) Severe palmar pallor,
4) Eye signs of vit A deficiency (dry conjuctiva or cornea, bitots spots, corneal ulceration,
keratomalacia),
5) Localizing signs of infections(skin infections or pneumonia),
6) Signs of HIV infection,
7) Fever/hypothermia,
8) Mouth ulcers,
9) Skin changes of kwashiokor (hypo/hyperpigmentation, desquamation, ulceration spreading over
limbs, thighs, genitalia, groin and behind the ears, exudative lesions resembling severe burns
often with secondary infection.
Rx. General Rx.
1. Separate child from infected children,
2. keep the child warm, minimize washing the child,
3. if necessary wash and dry him quickly.
Management of malnutrion: 2 phases ie stabilization and rehabilitation.
10 steps:
1. Hypoglycemia,
2. Hypothermia,
3. Dehydration,
4. Electrolyte imbalance,
5. Infection,
6. Micronutrients,
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7. Initiate feeding,
8. Catch up growth,
9. Sensory stimulation,
10. Prepare for follow up.
1. Hypoglycemia: check blood glucose, if <3mmol/l give 50mls of 10% glucose, if child is
uncounvious give IV glucose 10% 5ml/kg or sucrose solution, follow this by feeding.
2. Hypothermia: dx. axillary temp of <35ºc and rectal temp of 35.5ºc, feed immediately, cover with
warm clothes, place a heater or lamp nearby, skin by skin care can be done, give appropriate
antibiotics, monitor rectal temp 2 hrly.
3. Dehydration: dry oral mucosa, do not use IV fluids unless child in shock, give RESOMAL orally5-
10ml/kg/hrin 4-10 hrs, monitor RR, HR, urine output, vomit frequency of stool and vomit.
4. Electrolyte imbalance: give K+ ang Mg2+, avoid Na+ as it worsens edema and precipite heart
failure.
5. Infections: broad spectrum antibiotics eg cotrimoxazole, ampicillin, gentamycin, penicillin,
measles vaccine if child older tha 6 months, delay vaccination if child in shock, treat for warms
with mebendazole.
6. Micronutrients: daily for at least 2 weeks give; multivitamins, folic acid 5mgon day 1, the
1mg/day subsequently, zinc 2mg/kg/day, copper 0.3mg/kg/day, once gaining weight give ferrous
sulfate 3mg/kg/day, vit A orally <6 months 50000 IU, 6-12 months 100 000 IU, older children 200
000 IU a day.
7. Initial feeding: Day 1-2: energy of 100-130kcal/kg/day, protein of 1-2ng/kg/day, of F75,
11ml/kg/feed, 2 hrly. Day 3-5: energy of 130-160, protein of 2-3, F75/F100, 16 ml/kg/feed, 3hrly.
Day 6+: energy of 160-200, protein 4-6, F100, 22ml/kg/feed, 4hrly.
8. Catch up growth: return of appetite and edema is gone. Rx. Change F75 to F100, give child
unlimited amounts about 200kcal/kg/day, monitor for signs of heart failure.
9. Sensory stimulation: tender loving care, carefully stimulating environment, structured play 15-30
min daily, physical activity, maternal involvement if possible.
10. Preparation for follow up: give nutritional counc0selling on good feeding practices and sensory
stimulation, frequent feeding with energy rich and nutrient dense foods.
Mangement of co-morbidities:
1) Severe anemia- Hb <4g/dl, blood tranfusion,
2) Dermatosis of kwashiokor- apply barrier cream eg petroleum jelly, zinc and castor oil drops,
3) Diarrhea- give metronidazole incase of giardia lambia,
4) Tuberculosis- perform mantoux test and CXR the treat accordingly.
5) Weight gain: should be monitoured as follows: poor <5g/kg/day, moderate 5-10g/kg/day, good
> 10g/kg/day.

104.Criteria of admitting patient with pneumonia (Use CURB-65 score)

105.Most common diseases of children in Kenya(

1. malaria,
2. neonatal sepsis/jaundice,
3. meningitis,
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4. pneumonia,
5. bronchiolitis
6. gastroenteritis,
7. malnutrition,
8. TB, asthma,
9. Prematurity

106.Burns classification and management

A. According to cause:
1. Thermal,
2. Caustic chemicals or acid,
3. Electricburns,
4. Frostbite,
5. Mechanical/frictional burns,
6. Radiation injury.
B. According to depth of injury:
1. 1st degree ie epidermis only,
2. 2nd degree:
a) superficial-epidermis+upper 1/3 of dermis,
b) deep- epidermis+upper 2/3 of dermis,
3. 3rd degree/full thickness burn: full epidermis+dermis,
4. 4th degree: muscle involvement,
5. 5th degee: bone involvement.
C. According to size of burn:
wallace rule of 9s:
A. Minor burn:
young and old<10%,
adult <15%,
3rd degree <1%.
B. Moderate burn:
young and old <10-15%,
adult 15-25%,
3rd degree <2-5%.
C. Severe burn:
young and old > 15%,
adult > 25%,
3rd degree > 5%.
Management: indications for admission:
A. Causes: electrical, chemical.
B. Severity: moderate and severe, 3rd and 4th degree, non healing after 14-21 days.
C. Anatomical location: head, neck, palms, soles and perineum, circumferential limb burn, burns of the
back, all inhalation injury.

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D. Patient factors: extreme of ages <4> 50, burns of both limbs in an obese pt, pregnancy, burn with
trauma, victims with preexisting medical disorders eg DM, epilepsy, deaf, blind, infection.
Rx. First 48 hrs:
1. Primary survey ie ABCDE, large bore IV, catheter, NGT, intubation if inhalation burn.
2. Secondary survey: hx of burn, calculate BSA.
3. Medical management:
i. Fluid using parklands formular 4xkgxBSA,
ii. Give half in first 8 hrs, 50% more if electrical burn,
iii. Monitor urine output normal 30-50ml/hr,
iv. If electrical burn 100ml/hr to flush the kidneys
v. Nutrition use curreri formular 25 kcla/kg+( 40kcalxTBSA).
vi. 48hrs to 6 months: do escharotomies.
Complications:
A. Instant: inhalation injury and dehydration,
B. Immediate hours: haemorrhage, airway obstruction and circulatory collapse,
C. Early complications: anemia, electrolyte imbalance, infections, ARDS

107.Description of an X-ray
Pts Name, Sex and Date taken.
Comment on technical quality i.e
P Position,
I Inspiration,
R Rotation
E Exposure.
Then ABCDEF i.e
1. Airway,
2. Bones,
3. Cardiac silhouette,
4. Diaphram,
5. Effusion,
6. Filelds,
7. Lines, tubes, devices, surgeries.

108. DVT causes in pregnancy

1) Risk factors-had thrombosis before,
2) Age over 35,
3) Thrombophilia,
4) Obese BMI > 30,
5) Twin or more gastation,
6) On fertility treatment,
7) CS,
8) Sitting still for long periods of time,
9) Smoker,
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10) Dehydration,
11) Premature delivery,
12) Maternal cardiac disease,

109. Indication of dialysis

In acute kidney injury; mnemonic AEIOU,
Acidemia from metabolic acidosis where correction with sodium bicarbonate is impractical and result
in fluid overload.
Electrolyte abnormality, eg severe hyperkalemia,
Intoxication, acute poisoning with a dializable substance, ie SLIME salicylic acid, lithium, isopropanol,
magnesium conataining laxatives, ethyline glycole.
Overload of fluid not expected to respond to treatment with duretics.
Uremia complications, eg pericarditis, encephalopathy, gastrointestinal bleeding.
Chronic kidney disease, GFR of <10 ml/min.

110. Investigation in bowel obstruction

Intestinal obstruction:
failure, reversal or impairment of the normal transit of intestinal content.
Classification and etiology:
A.Dynamic obstruction: failure of peristalsis.Causes:
1. Neuronal defect e.g spinal injury.
2. Electrolyte imbalance ie hypokalemia, acid base imbalance, uremia.
3. Ischemic causes ie venous or arterial defects.
4. Infections eg peritonitis.
5. Retroperitoneal hematomas.
B.Mechanical obstruction:
1. Luminal lesions: impactions, gallstones, bezoares and other foreign matter, meconium in
newborns, intussusception in infants.
2. Intramural lesions:
a) congenital eg atresia and stenosis, imperforate anus, deplications, meckels diverticulum,
b) trauma,
c)inflammatory e.g crohns disease, diverticulitis, ulcerative colitis, radiation, toxic ingestion,
d) neuromascular defect e.g megacolon, neuromyopathic mortility disorders,
e) neoplastic.
3. Extrinsic lesions:
a. adhesions,
b. hernia,
c. masses e.g annular pancreas, anomalous vasculature, abscess and hematoma, neoplasms.
d. volvulus,
Symptoms and signs:
triad of symptoms:
1. Abdominal cramps are centered around the umbilicus or in the epigastrium, if cramps become
severe and steady, strangulation probably has occured.
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2. Vomiting starts early with small bowel and late with large bowel obstruction.
3. Constipation if complete obstruction, diarrhea may occur with pertial obstruction.
Dx.
Inspection- distention, rigid abdomen, scars, hernia, visible peristalsis, visible masses. Palpation-
tender, rigid, palpable masses.
Percussion: resonance.
Auscultation: absent sound in paralytic ileus, hyperactive sound in mechanical obstruction.
Examination of inguinal and femoral regions: hernia. DRE: hard stool suggests impaction, soft stool
suggests constipation, an empty vault suggests obstruction proximal to the examining finger. Fecal
occult. Do a VE when appropriate. Examine the chest.
Labs:
1. FHG: leucocytosisand also acidosis shows strangulated, intravascular volume deplition,
2. Electolytes.
3. UECs.
Imaging:
1. Abdominal series ie supine and erect AXR-dilated loops of bowel, air fluid levels, a paucity of air in
the colon.
2. Contrast AXR can be used to distinguish mechanical obstruction fron ileus and pertial from
complete obstruction. If perforation is suspected use water soluble contrast rather than barium.
3. CT scanning is indicated in selected cases.
Rx.
1. NG tube for decompression,
2. IV fluids,
3. Catheterize and monitor input/output,
4. Visualization of foreign material,
5. Profilactic antibiotica,
6. Soapy enema in partial distal obstruction.
Surgical management:
Indication:
1. Peritonism,
2. Continued deterioration of pts condition. Closed procedures e.g lysis of adhesions, reduction of
intussusception, reduction of volvulus, reduction of incarcerated hernia. Enterotomy for removal of
bezoars, foreign bodies, gallstones. Resection of bowel for obstructing lesions, strangulated bowel.
Bypass of intestine around obstruction. Enterocutaneous fistula proximal to obstruction ie colostomy,
cecostomy.

111. Post mastectomy care

1.pain management-control pain with vicodin or ibuprofen or tilenol, put ice packs it can reduce
swelling and discomfort.
2. Incision and dressing care: remove dressing after 10 days, stitches after 2 weeks. Empty the drain 2-
3 times a day or when it is full.the tube is removed after a few days.
3. Activity: limit shoulder movement/lifting of the arm above 90º untill after the drains are removed to
decreases risk seroma, phsiotherapy to regain movement and flexibility.
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4. Diet: IV remains in place untill the pt can tolerate oral liquid the slowly progress to solid food.
5. Follow up care.
When to contact the doctor:
1. pain not relieved by meds,
2. fever,
3. exessive bleeding,
4. exessive swelling,
5. discharge or bad odour.
Complications of mastectomy: infection, lymphedema and seroma.

112. Ddx for Ring enhancing lesions

Tumour:
a) primary brain tumour eg anaplastic astrocytoma,
b) Metastatic eg lung., Pus/abscess: pyogenic brain abscess, fungal ie cryptococcus, candidiasis,
nocardiosis, parasitic ie toxoplasmosis. or Blood: subacute hematoma with capsule.
Others: TB, granuloma, MS, radiation necrosis, lymphoma, trauma, infarct. )
Mneumonics MAGIC DR:
Metastasis,
Abscess,
Glioblastoma multiforme,
Infarct(subacute phase),
Contusion,
Demyelinating disease e.g tumefactive MS,
Radiation necrosis.

113.Portal hypertension Elevation of hepatic venous pressure gradient to> 5mmhg.

Causes:
1. Prehepatic: portal vein thrombosis, congenital atresia.
2. Intrahepatic: liver cirrhosis, hepatic fibrosis due towillsons disease, hemochromatosis or congenital
fibrosis, schistosomiasis, massive fatty change and diffuse granulomatous diseases e.g sarcoidosis,
milliary TB.
3. Posthepatic: obstruction causes e.g hepatic vein thrombosis, inferior vena cava thrombosis, IVC
congenital malformations and constrictive pericarditis.
Signs and symptoms:
1) Ascites,
2) Hepatic encephalopathy,
3) Increased risk of spontaneous bacterial peritonitis,
4) Increased risk of hepatorenal syndrome,
5) Splenomegaly,
6) Portocaval anastomoses ie esophageal varices,
7) Gastric varices,
8) Anorectal varices and caput medusae.
Dx.
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1. Hepatic venous gradient (HVPG)> 5mmhg.

2. Clinically significant if > 10 to12 mmhg.
Rx.
1. Transjugular intrahepatic portosystemic shunt(TIPS),
2. prophylaxis of variceal bleeding,
3. management of active variceal bleeding,
4. management of ascites ie diuretics,
5. control of hepatic encephalopathy ie lactulose.

114.Cyanosis peripheral and Central DDX

Causes of Peripheral cyanosis:
1) exposure to cold,
2) severe hypotension,
3) Raynaulds phenomenon,
4) venous obstruction.
Causes of central cyanosis:
1. Respiratory failure,
2. Cyanotic heart diseases ie
i. Truncus arteriosus,
ii. Tetrology of falot,
iii. Tricuspid atresia,
iv. Transposition of aorta,
v. Total anomolous venous return.

115.CCF
Failure of the heart to pump blood effectively.
Types:
LHF caused by pulmonary congestion.
RHF caused by venous congestion.
Causes: MI, pulmonary embolus, dysrhythmia, thyrotoxicosis, viral, alcohol. Signs:
LHF:
1. orthopnoe,
2. paroxysmal noctural dyspnea,
3. rales,
4. dyspnoe on exertion,
5. caugh,
6. nocturia,
7. S3 gallop,
8. diaphoresis,
9. tachycardia.
RHF:
1) RUQ pain,
2) Hepatomegaly,
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3) hepatojugular reflex,
4) JVD,
5) Ascitis,
6) Cyanosis,
7) peripheral edema.
Dx:
1. CXR,
2. EchoCardiography.
Mx:
1) Non pharmacologic: Na and H2O restriction.
2) Pharmacologic: first line ACE inhibitors, diuretics, beta blockers, digoxin, spironolactone.)

116.Leishmaniasis
zoonotic infection, protozoa leishmania, transmitted by sand flies -phlebotomous.
Types:-
1. Cutaneous caused by L. tropica L. brasiliens
2. Visceral or kala azar caused by L. donovani.
It is an intracellular parasite, reservior in india is humans, in africa is rodents.
Life cycle: 2 forms amastigote in human promastigote in sand flies.
Methods of transmission:
bite of sand flie. It supresses cell immunity.
Clinical presentation;
1) Leishmanioma ie ulcer of bite site,
2) Fever, night sweats,
3) Late presentation ie oedema,
4) Haemorrhage,
5) Growth failure,
6) General malaise,
7) Abdominal swelling ,
8) Discomfort,
9) Pancytopenia/hepatic failure,
10) Skin hyperpigmentation,
11) Caugh.
Physical exam;
1. pallor,
2. jaundice,
3. splenomegally,
4. hepatomegally,
5. dry skin,
6. lymphadenopathy.
Post kala azar dermal leishmaniosis:
a) depigmented macules,
b) erythematous patches,
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c) yellowish pink nodules.

Cutaneous leishmaniosis:
Oriental sores ie L. tropica, american cutaneous ie L. brasiliensis, face, arms and legs.
Lesions are not destructive or errossive but disfiguring.
Mucocutaneous leishmaniasis:
mucocutaneous junction around the nose.
Investigations:
1) FHG ie pancytopenia,
2) Elevated gamma globulins,
3) Reverse albumin globulin ratio,
4) Direct evidence of infection,
5) Smear ie thick film by centrifuging,
6) Culture NNN media,
7) Detection of hypergammaglobulinemia,
8) Immunological tests eg IFA, PCK, PCR,
9) Leishmania skin test ie montenegro test.
Manamgement:
1. diet,
2. blood transfusion,
3. treat secondary infection,.
4. Sodium stibogluconate,
5. amphotericin B
6. deoxycholate,
7. miltefosine.

117.Postpartum hemorrhage
Loss of blood>500 afterSVD or > 1000 after CS.
Types:
1. Primary PPH i e first 24 hours, and
2. Secondary PPH beyond 24 hours.
Causea: 4Ts.
1. Tone: atony. Risk factor of atony; urinary retention, grand multiparity, multiple gastation,
polyhydramnios, chorioamnionitis, general anaestesia, MgSO4 therapy, precipitous delivery,
prolonged labour.
2. Tissue: retained placenta tissue. Risk factors; placenta praevia/accreta, cord avulsion, preterm
delivery, succenturiate lobe, previous uterine scar, manual extraction of the placenta.
3. Trauma: vaginal, cervical,perineal laceration, uterine inversion. Risk factors; operative vaginal
delivery, improper episiotomy, excessive cord traction, uterine rapture.
4. Thrombotic: coagulation disorder. Risk factors; uterine fetal demise, placenta abruptio, placenta
praevia, preeclampsia/eclampsia, Hellp syndrome.

118. Glasgow coma scale score:

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Score Eye open Best motor response Best verbal response

(> 8
6 - Obey command -
5 - Localize pain Oriented
4 spontaneously Flexion withdrawal Confused
3 To speech Decelerate extension Inappropriate words
2 To pain Decorticate flexion Incomprehensive sounds
1 Never No response silent
severe head injury ,8-12 moderate ,13 -15 mild head injury)

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