1. Overtime, this condition worsens and persists in 8.

What primary cause of atherosclerosis is

which the blood vessel wall becomes inflamed mentioned in the following?
and eventually gets injured potentially leading to a. Genetics
CVS problems. b. Chronic inflammation and buildup of plaque
a. Atheroma c. Aging
b. Atherosclerosis d. Stress
c. Atheromatous plaque
d. Atherogenesis 9. A common symptom of atherosclerosis is
a. Sudden loss of vision
2. During lipid transport, fats are absorbed in GI b. Chest pain or angina
and packaged which transport triglycerides or c. Hearing loss
dietary fats from the small intestines to various d. Persistent cough
tissues in the body for energy and storage. After
they have delivered the triglycerides to tissues, 10. What is the role of HDL in atherosclerosis?
they are being taken up by the liver for further a. It promotes the buildup plaque in arteries
metabolism. b. It transports cholesterol away from the
a. VILDL arteries to the liver
b. ApoB-100 c. It has no significant role in atherosclerosis
c. LDL d. It acts as structural protein in arterial walls
d. Chylomicrons
11. In an accelerated type of hypertension we have
3. Are attributed in helping to prevent this to rapidly reduce the BP over 24 to 36 horse less
progressive chronic inflammatory disease of the than 150/90mmHg
blood vessels. a. True
a. LDLs b. False
b. VDLs c. Depends
c. Foam cells d. Maybe
d. HDLs
12. Which of the is a common risk factor for
4. In fatty streak formation, there is fat deposition developing hypertension?
under the tunica intima layer, the yellowish color a. Strenuous exercise
reflects: b. High sodium diet
a. Oxidized lipids c. Family history of hypertension
b. Presence of foam cells d. High potassium intake
c. Both d Neither
13. Hypertension can lead to damage in which of the
5. This gradual, persistent disease or condition is following organs?
characterized by the narrowing of the arteries. a. Lungs
Narrowing is to b. Kidneys
a. Thrombosis c. Pancreas
b. Arteritis d. Small intestine
c. Stenosis
d. Embolism 14. The happens during myocardial ischemia
a. Increased level of lactate
6. Which of the following is NOT a common risk b. Arrhythmia
factor this condition wherein there can be c. Tachycardia
formation of complicated plaque d. AOTA
a. High blood pressure
b. Smoking 15. This is a type of angina that is marked by
c. Low levels of triglycerides neuropathy, and is usually painless
d. Diabetes a. Pre-infarction
b. Prinzmetal
7. The primary cause of “gruel” and “hardening” c. Stable
a. A diet low in cholesterol d. Silent
b. High levels of cholesterol
c. The buildup of fatty deposits in arterial walls
d. Regular exercise
16. This is characterized by a recurrence of chest 24. A type of shock where there is can be massive
pain that is unrelated to activity pulmonary embolism, cardiac tamponade an/or
a. Stable angina tension pneumothorax
b. Prinzmetal angina a. Cardiogenic shock
c. Unstable angina b. Distributive shock
d. Silent ischemia c. Obstructive shock
d. Hypovolemic shock
17. This type of angina highly suggests that an
myocardial infarction is about to happen 25. The correct sequence of cough reflex
a. Unstable angina a. Irritation, inspiration, compression, expulsion
b. Variant angina b. Expulsion, inspiration, irritation, compression
c. Silent ischemia c. Irritation, compression, inspiration, expulsion
d. Stable angina d. Inspiration, irritation, compression, expulsion

18. Seen in angina pectoris 26. The following are signs of labored breathing on
a. Fear of impending doom children except
b. Crushing, retrosternal chest pain for <15 mins a. Alar flaring
c. Pulmonary congestion b. Subcostal retraction
d. AOTA c. Intercostal retraction
d. Tachycardia
19. The defunctive treatment of angina
a. Decompensation 27. A 36 yr old factory worker has been coughing for
b. Revascularization 4 weeks. He is clinically classified to have
c. Catheterization a. Acute cough
d. Cauterization b. Subacute cough
c. Chronic cough
20. Which causative agent causes tonsillopharyngitis d. Allergic cough
can lead to rheumatic fever
a. Strep pneumoniae 28. The following are criteria for chronic bronchitis
b. strep pyogenes EXCEPT
c. strep bovis a. Persistent cough with sputum production
d. strep agalactiae b. At least 3 months
c. At least 2 consecutive years
21. One criterion is not included in the choices d. With identifiable cause
a. Fever
b. Migratory polyarthritis 29. This refers to irreversible enlargement of the
c. Pericarditis airspaces distal to the terminal bronchioles,
d. Sydenham chorea accompanied by destruction of their walls
a. Bronchial asthma
22. Choose the correct match for the criteria of acute b. Bronchiectasis
rheumatic fever c. Chronic bronchitis
a. Fever + Tachycardia +positive throat swabs d. emphysema
culture
b. Anti-DNase B antibodies + erythema 30. This type of emphysema is typically seen in
marginatum + limited ESR smokers. Only respiratory bronchioles are a ected
c. Anti-streptolisin-O + Subcutaneous nodules + and it a ects the upper lung zone.
carditis a. Panacinar
d. Prolonged pr segment + arthralgia + fever b. Centriacinar
c. Chronic bronchitis
23. Choose the correct one to fulfill the criteria for d. Pneumonia
acute rheumatic fever
a. Anti streptolysin-O titer + positive throat
swabs culture + fever
b. Sydenham chorea + Painless nodules +
Anti-DNase B antibodies
c. Carditis + arthralgia + positive throat swabs
culture
d. Elevated ESR + fever + arthralgia
 PATHOPHYSIOLOGY

MODULE 9 OUTLINE

I. Lithiasis
a. Nephrolithiasis
b. Urolithiasis
II. Common infections of the Renal System
a. Pyelonephritis
b. Cystitis
c. Gonococcal and Non-Gonococcal
Urethritis
III. Glomerular Diseases
a. Nephritic Syndrome
b. Nephrotic Syndrome
IV. Renal Failure
a. Acute
b. Chronic

LITHIASIS
NEPHROLITHIASIS & UROLITHIASIS

Etiology:Most common cause of Lithiasis - Calcium stone

- Hypercalcemia (Eg. Inc intake, or Hyper-PTH) > Calcium Stones 80%
- Chronic UTI > Triple Phosphate /Struvite/ “Staghorn” Stones 15%
- Uremia > Urate Stones (+ Gout)

Pathogenesis:
- Hypercalcemia > Calcium in Urine Precipitates out of Solution > Calcium Stones 80%
- Chronic UTI > Gram-Neg Rods (Proteus, Pseudomonas & Klebsiella - NOT E. coli) > Triple
Phosphate/Struvite/ “Staghorn” Stones 15%
- May cause > Urinary Obstruction > Hydronephrosis > Stretching of Renal Capsule > Pain)

Morphology:
a. Calcium Stones 80%
- Small, hard Stones (1-3mm);
- Stones have sharp edges
- Radio-Opaque
b. Triple Phosphate/Struvite/ “Staghorn” Stones 15%
- Large Stones (Molds to Renal
Pelvis/Calyces) ʹ Hence Staghorn͘͟
- Chronic Irritation of Epithelium surrounding Stone > Squamous Metaplasia

Clinical Features:
- Usually, Unilateral o Painful Hematuria ʹ Macro/Micro
- Writhing in pain͕ pacing about and unable to lie still͟
 - Hydronephrosis > Stretching of Renal Capsule > Flank Pain & Tenderness.
o Stone in Ureteropelvic Junction > Deep flank pain. No radiation. Distension of the Renal Capsule.
o Stone in Ureter > Intense, Colicky Pain (Loin > Inguinal Region > Testes/Vulva) + N/V.
o Stone in Ureterovesical Junction > Dysuria, Frequency, + Tip of penis pain
Complications:
- Hydronephrosis
- Post-Renal Failure
- Infection >ʹ (UTI/Pyelonephritis/Perinephric Abscess)
Investigations:
- Abdo USS – (Confirm Stone)
- Abdo XR – (Confirm Calcium Vs Radio-Lucent Stone)
- UECs – inc. Calcium or inc. Urea
Management:
- Conservative – (Daily Na-Bicarbonate Tablets to Alkalize Urine > Dissolve Urate Stones)
- (ESWL) Extracorporeal Shock-Wave Lithotripsy - (For Calcium Stones)
- Surgical – (For All Stones Not Amenable to the above)
Location of Stones
a. calyx
- may cause flank discomfort, recurrent
infection or persistent hematuria
- may remain asymptomatic for years and
not require treatment
b. pelvis
- tend to cause UPJ obstruction renal pelvis and one or more calyces
c. staghorn calculi
- often associated with infection
- infection will not resolve until stone cleared
- may obstruct renal drainage
d. ureter
- 5 mm diameter will pass spontaneously in 75% of patients the three narrowest passage points for upper
tract stones include: UPJ, pelvic brim, UVJ

Stone Pathogenesis
Factors promoting stone formation
- stasis (hydronephrosis, congenital abnormality)
- medullary sponge kidney • infection (struvite stones)
- hypercalciuria
- increased oxalate
- increased uric acid
Loss of inhibitory factors
- magnesium (forms soluble complex with oxalate)
- citrate (forms soluble complex with calcium)
- pyrophosphate
- glycoprotein

STONE TYPES
1. Calcium Stones
- Account for 80 - 85% of all stones
- Ca2+ oxalate most common, followed by Ca2+ phosphate description
- grey or brown due to hemosiderin from bleeding
- radiopaque
2. Struvite Stones
- Female patients affected twice as often as male patients
- Etiology and pathogenesis
o account for 10% of all stones
o contribute to formation of staghorn calculi
o consist of triple phosphate (calcium, magnesium, ammonium)
o due to infection with urea splitting organisms NH2CONH2 + H2O ––> 2NH3 + CO2
o NH4 alkalinizes urine, thus decreasing solubility
- Common organisms
 o Proteus
o Klebsiella
o Pseudomonas
o Providencia
o S. aureus
o not E. coli

Treatment
- Complete stone clearance (ESWL/percutaneous nephrolithotomy)
- Acidify urine, dissolve microscopic fragments
- Antibiotics for 6 weeks
- Follow up urine cultures

3. Uric Acid Stones

- Account for 10% of all stones
- Description and diagnosis
o orange colored gravel, needle shaped crystals
o radiolucent on x-ray
o filling defect on IVP
o Radiopaque on CT scan
o Visualized with ultrasound
Etiology
o hyperuricosuria (urine pH < 5.5)
o secondary to increased uric acid production, or drugs (ASA and probenecid)
o hyperuricemia
o gout
o myeloproliferative disease
o cytotoxic drugs
o defect in tubular NH3 synthesis (ammonia trap for H+)
o dehydration, IBD, colostomy and ileostomy
Treatment
o increase fluid intake
o NaHCO3 (maintain urinary pH no less than 6.5)
o allopurinol
o avoid high protein/purine diet

4. Cystine Stones
- Autosomal recessive defect in small bowel mucosal absorption and renal tubular absorption of dibasic
amino acids
- Seen in children and young adults
- Aggressive stone disease
- Description
o hexagonal on urinalysis
o yellow, hard
o radiopaque (ground glass)
o staghorn or multiple
o decreased reabsorption of “COLA”
o cystine (insoluble in urine); ornithine, lysine, arginine (soluble in urine)

Diagnosis
o amino acid chromatography of urine ––> see COLA in urine
o serum cystine
o Na+ nitroprusside test
Treatment
o greatly increase water intake ––> 3-4 L urine/day
o HCO3–
o decrease dietary protein ––> methionine
o penicillamine chelators ––> 2 g daily, soluble complex formed; use cautiously
o a-mercaptopropionylglycine (MPG) ––> similar action to penicillamine, less toxic
o captopril (binds cystine)
o Irrigating solutions: N-acetylcysteine (binds cystine), Tromethamine-E

III. COMMON INFECTIONS OF THE URINARY SYSTEM

a. Pyelonephritis

1. Acute Pyelonephritis
- Infection of the renal parenchyma with local and systemic manifestations of infection
- may be classified as uncomplicated or complicated
o uncomplicated: in the absence of conditions predisposing to anatomic or functional impairment of
urine flow
o complicated: occurring in the setting of renal or ureteric stones, strictures, prostatic obstruction
(hypertrophy or malignancy), vesicoureteric reflux, neurogenic bladder, catheters, DM, sickle-
cell hemoglobinopathies, polycystic kidney disease, immunosuppression, and post-renal
transplant
Etiology
- Usually ascending microorganisms, most often bacteria
- in females with uncomplicated pyelonephritis usually E. coli
- causative microorganisms are usually E. coli, Klebsiella, Proteus, Serratia, Pseudomonas, Enterococcus,
and S. aureus
- If S. aureus is found, suspect bacteremic spread from a distant focus (e.g. septic emboli in infective
endocarditis) and suspect (possible multiple intra-renal micro abscesses or perinephric abscess)

Clinical Presentation
- Rapid onset (hours to a day)
- Lethargic and unwell, fever, tachycardia, shaking, chills, nausea and vomiting, myalgias
- Marked CVA or flank tenderness; possible abdominal pain on deep palpation
- Symptoms of lower UTI may be absent (urgency, frequency, dysuria)
- May have symptoms of Gram-negative sepsis Eto answer dun kase ang
Laboratory Investigations tanong ay EXCEPT eh
- Urine dipstick: +ve for leukocytes and nitrites, possible hematuria
- Microscopy: > 5 WBC/HPF in unspun urine or > 10 WBC/HPF in spun urine, bacteria ang ang nakalagay dun
- Gram stain: Gram negative rods, Gram positive cocci ay gram posutive rodes
- Culture: > 105 colony forming units (CFU)/mL in clean catch midstream urine or > 102 CFU/mL in
suprapubic aspirate or catheterized specimen
- CBC and differential: leukocytosis, high % neutrophils, left-shift (increase in band cells - immature
neutrophils)
- Blood cultures: may be positive in 20% of cases, especially in S. aureus infection
- Consider investigation of complicated pyelonephritis:
o if fever, pain, leukocytosis not resolving with treatment within 72 hr, if male patient, or if there is
history of urinary tract abnormalities (abdo/pelvis U/S, CT for renal abscess, spiral CT for
stones, cystoscopy)
Treatment
- Uncomplicated pyelonephritis with mild symptoms
o 14-day course of TMP/SMX or fluoroquinolone or third generation cephalosporin
o Start with IV for several days and then switch to PO (can then be treated as outpatient)
- Patient more than mildly symptomatic or complicated pyelonephritis in the setting of stone obstruction is a
urologic emergency (placing patient at risk of kidney loss or septic shock)
o start broad spectrum IV antibiotics until cultures return (imipenem or meropenem or piperacillin
/tazobactam or ampicillin plus gentamicin) and treat 2-3 weeks
o follow-up cultures 2-4 weeks after stopping treatment
- If no improvement in 48-72 hr, need to continue on IV antibiotics, assess for complicated pyelonephritis or
possible renal or perinephric abscess
Prognosis
- Treated acute pyelonephritis rarely progresses to chronic renal disease
- Recurrent infections often constitute relapse rather then re-infection

2. Chronic Pyelonephritis

- A form of chronic tubulointerstitial nephritis of bacterial origin

- Cortical scarring, tubulointerstitial damage, and calyceal deformities seen
- May be active (persistent infection) or inactive (persistent focal sterile scars post-infection)
- Histologically indistinguishable from many other forms of TIN (severe vesicoureteral reflux, hypertensive
disease, analgesic nephropathy)
- Active chronic pyelonephritis may respond to antibiotics
- Need to rule out TB

III. GOMERULAR DISEASES

a. NEPHROTIC SYNDROMES
(Incomplete Glomerular-Membrane Damage)

Clinical Features
- Normal GFR
- +++Polyuria
- ++++ Proteinuria (>3000mg/day: Nephrotic)
o > Granular (Protein) Casts.
o > Edema (Especially Periorbital)
o > Hypercoagulability (Loss of Antithrombin-III in Urine)
o > Immunocompromise state (Loss of Ig in Urine)
o Hyperlipidemia (Attempted Hepatic Compensation for dec. Plasma Osmolarity)
- Serum Creatinine Mildly Elevated
o (Dehydrated due to Polyuria; But Edematous due to Proteinuria)

The following are nephrotic

syndromes EXCEPT:
1. MCD (Minimal Change Disease) / Foot Process Disease/ Nil Disease)
- MCD = THE Childhood cause of Nephrotic Syndrome (1-8yrs)
Etiology:
- Post-Infective (URTI)
Clinical Features:
- Eg. 2yo Boy with sudden onset Polyuria, Oedema & Proteinuria following URTI.
- Children (1-8yrs)
- Prognosis - Spontaneous Remission <70% of patients; Some may progress to FSGS

2. MGN (Membranous Glomerulonephrosis):

- MGN = >50% of Adult Nephrotic Syndrome: *Note: tandaan din yung alternative
names sa bawat diseases
Etiology
- Autoimmune - Ag:Ab Complex Deposition E.g. Foot process disease, Nil Disease
Clinical Features:
- Eg. 35y female, Tired for years, Worsened for two months. She has noted swelling of her legs and
puffiness around eyelids (Periorbital edema - A classic sign of nephrotic syndrome).
- Adults - 40-60yrs
- Nephrotic Syndrome - Polyuria, +++ Proteinuria, edema.
- Prognosis - Good, but Occasionally progresses to ESRD

3. FSGS (Focal Segmental Glomerulosclerosis):

- <35% of Adult Nephrotic Syndrome

 - Vey similar to MCD but in adults

Etiology: Same as MCD

- Often a recent history of an URTI
Clinical Features:
- Eg., 49 y/o Nephrotic Syndrome, non responsive
- Nephrotic Syndrom - +++ Selective Proteinuria
- Prognosis – Poor: 30% Remission; 50% CKD and 20% RPGN

b. NEPHRITIC SYNDROMES
(Complete Glomerular-Membrane Damage)

Clinical Features of Nephritic Syndrome:

- Dec GFR
- Oliguria
o > Renal Hypertension (Hypoperfusion of JG Cells due to dec GFR)
o > Fluid Overload Edema: (dec Plasma Osmolality & Na + H2O Retention)
- Microalbuminuria
- ++++ Hematuria
o > RBC (Cellular) Casts.
o > Anemia
- Inc. Creatinine Question: The following are
nephritic syndromes EXCEPT:
Fluid Overloaded due to Oliguria; And Edematous due to Fluid Overload)

1. PSGN (Post-Strep Glomerulonephritis)

- PSGN = THE Childhood cause of Nephritic Syndrome (3-15yrs)

- Eg. 8-year-old girl with fever, oliguria, smoke colored urine & hypertension following upper respiratory
tract infection.
Etiology:
- Post-Infective (GABH-Streptococcal Pharyngitis) Ag:Ab Complex Deposition
Clinical Features:
- Nephritic Syndrome - Oliguria, Painless Hematuria, Non-Selective Proteinuria, Edema, Hypertension
Prognosis:
- Good Prognosis in Children (But progressive in adults)

2. IgA Nephropathy (Berger’s Disease)

- IgA-Nephropathy = THE Adult (15-30yrs) Cause of Nephritic Syndrome
- Eg. 18y male Recurrent, Episodic Painless +++Hematuria, 3-6 days, usually following URTI.
Etiology:
- Autoimmune - Ag:IgA Complex Deposition in Glomerulus
Clinical Features:
- Nephritic Syndrome - Oliguria, Painless Hematuria, Non-Selective Proteinuria, edema, Hypertension
- High Serum IgA

Prognosis:
- 30% > Slowly Progressive
- 10% > Renal Failure

3. RPGN (Rapidly Progressive Glomerulonephritis):

- RPGN = NOT a Separate Disease; ANY Glomerulonephritis can > RPGN
Etiology:
- Progression of any Glomerulonephritis (Autoimmune)

Pathogenesis:
- Rapidly Progressing Glomerulonephritis > Renal Failure within Weeks.
Clinical Features:
- Nephritic Syndrome - Oliguria, Painless Hematuria, Non-Selective Proteinuria, Oedema, Hypertension
Prognosis:
 - Poor: Quickly progresses to ESRF

IV. RENAL FAILURES

a. Acute Renal Failures

Acute Renal Failure - General Information: Etiology:

- Rapid loss of kidney function͟

1. Pre-Renal Renal Failure:

- Before the Blood Reaches the Kidney (Ie. Dec. Glomerular Perfusion)
o Hypovolemia (Eg. Blood Loss)
o Decreased cardiac output (Eg. Heart Failure)
o Renal artery obstruction (Eg. Embolism)
2. Intra-Renal Renal Failure - The kidney itself is damaged
- Acute glomerular nephritis
- Tubular diseases e.g., acute tubular necrosis
- Interstitial diseases e.g., auto immune disorders such as SLE
- Vascular diseases e.g., polyarteritis nodosa

3. Post-Renal Renal Failure

- Due to outflow obstruction from the kidneys
o Cancer - Bladder / Prostate / Ureteric / Cervical
o Blood clot
o Calculi (Kidney stones - Bilateral)
o Accidental surgical ligation
Clinical Features:
- Uremia - (Fatigue, Malaise, Anorexia, Headache, Nausea, Vomiting)
- Hyperkalemia > Brady-Arrhythmias \
- Fluid Retention > Oedema (Peripheral & Pulmonary)
o RARELY, Hypertension & Cardiac Tamponade.
- Hematuria - Painless (Cancer) or Painful (Stones/LUTS)
- Flank pain (in specific conditions - Particularly Inflammatory or Ischemic)

4 Stages of Chronic Renal Failure

Stage 1 = > 90 ml/min GFR (Normal) plus other signs of renal disease

Stage 2 = 90-60 ml/min GFR

Stage 3 = 60-30 ml/min GFR

Stage 4 = 30-15 ml/min GFR

Stage 5 = <15 ml/min GFR

Clinical Complications of Renal Disease

- General Effects/Problems Encountered in Renal Failure: (Recall the functions of the kidney and then infer
what happens when they are eliminated!)
o Acid Base Balance (Renal Failure > Met. Acidosis)
o Electrolyte Balance (Renal Failure > Na+ & K+ Retention)
o Fluid Balance (Renal Failure > Fluid Overload)
o Dec Erythropoiesis (Renal Failure > Anemia)
o Renin Angiotensin System > Renal Hypertension
o Calcium Metabolism (Renal Failure > Osteoporosis & secondary Hyper-Parathyroidism)
o Uremia
o Dec Urine Output
o Dec Toxin Excretion (Renal Failure > Accumulation of Urea & Creatinine)
Investigations:
- Blood Urea: Creatinine Ratio - Distinguishing Between Intra/Pre/Post-Renal Failure:

Dec U:Cr = Intra Renal (Infection/toxin/Ischemia/Hypoxia/)

PATHOLOGIC KIDNEY!!

However, if:

Inc U:Cr = EITHER Pre Renal ( Hypotension/ Dehydration /Normal Kidney)

OR
Post Renal (BPH/Bladder Stone/Normal Kidney)

Urine Protein:Creatinine Ratio - Is there Proteinuria?

Interpretation:
- Daily Creatinine Excretion is Constant ͘ ͗ : inc P: CR = Inc Protein in Urine = Proteinuria

30-300mg = Microalbuminuria
>300mg = Macroalbuminuria/Proteinuria͟ >3000mg = Nephrotic Syndrome

b. Chronic Renal Failure

- Many etiologies: continuum of progressive nephron loss and declining renal function
- Asymptomatic until severe insufficiency develops
- Regional variation in leading causes worldwide
o In North America: diabetes (> 30%), hypertensive renal disease (23%), chronic GN (10%) (e.g.
IgA nephropathy), polycystic kidney disease (5%)
- Frequently patients present at end-stage with small, contracted kidneys, unknown etiology

Classification
- glomerular: primary or secondary glomerulonephritis
- tubulointerstitial disease (e.g., autoimmune interstitial nephritis)
- vascular (e.g., DM, HTN)
- hereditary (e.g. autosomal dominant polycystic kidney disease, Alport’s)

INDICATIONS FOR DIALYSIS IN CRF

- Maybe same as ARF
- more commonly = “dwindles”
o anorexia, nausea, vomiting, severe fatigue, pruritus, muscle cramps
o dialyze when creatinine clearance < 10% of normal (< 10 mL/min)
- diabetics less tolerant of uremia, dialyze when creatinine clearance < 15% of normal (< 15 mL/min)
- Prognosis: all with progressive renal failure progress to dialysis/transplant

******** END OF MODULE 8 ********

1
[MODULE 8 – NEUROLOGY ] Handout Prepared by: Michael Angelo Sumugat RMT, MD
PATHOPHYSIOLOGY: MODULE 7 - GASTROINTESTINAL QUIZ

1. Presence of gallstones - CHOLELITHIASIS

2. Associated with aids patient - CRYPTOSPORIDIUM

3. Most common hepatitis - HEP A

4. Post transfusion hepatitis - HEP C

5. Require the presence of Hep B - HEP D

6. Acute pancreatitis EXCEPT: Inc Amylase within 24 hrs, Inc Lipase after 72 hrs, Decreased
Bilirubin, Inc Alkaline Phosphatase - DECREASED BILIRUBIN

7. Acute pancreatitis symptoms: high grade fever, stress, hyperacidity - AOTA

8. Long-term immunity - ANTI HBS

9. Most common cause of chronic hepatitis - H. PYLORI

10. Fecal & Oral - BOTH HEP A&E

11. Acute and Chronic - HEP B&D

12. Vertical Transmission, HBsAg positivity, 6 weeks & 6 mos inc - HEP B

13. Hep B transmission: unprotected coitus, needles stick, blood transfusion - AOTA

14. Cause of Food Poisoning - STAPH AUREUS & BACILLUS CEREUS

15. Salmonella etiology - TYPHOID

16. Cholera - RICE WATER

17. Constipation - LACK OF DIETARY FIBER

18. Hemolytic - EHEC

19. Cessation of inspiration - MURPHY’S SIGN

20-23. All types of Worms

- Ascaris lumbricoides (roundworm)

- Trichuris trichiura (whipworm)
- Strongyloides stercoralis (threadworm)
- Ancylostoma duodenale (hookworm)

24. Mortality in Pregnancy - HEP E

25.