1.

Rheumatoid arthritis is autoimmune inflammation of synovium, which can cause damage to

cartilage and bones (symmetrical polyarthritis). Formation of pannus (proliferative granulation
tissue) causes articular cartilage and bone erosion.

2. In rheumatoid arthritis, systemic symptoms (fever, fatigue, weight loss) do happen.

Extraarticular manifestations (e.g. rheumatoid nodules in subcutaneous tissue and lung) are
common too. People living with RA can go back and forth between remission and relapse.

3. Rheumatoid factor is an IgM antibody that targets IgG’s Fc region. Anti-cyclic citrullinated
peptide antibody (ACPA) will also be present (more specific). Methotrexate is the most important
DMARD for treatment.

4. Diagnosis of acute rheumatic fever requires 2 major criteria (Jones) or 1 major + 2 minor
criteria (fever, arthralgia, elevated CRP/ESR, PR-interval prolongation).

5. Diffuse scleroderma is characterized by widespread skin involvement, rapid progression, early

visceral organ involvement. Catch with anti-scl-70 antibodies & anti-RNA polymerase III
antibodies.

6. Limited scleroderma—limited skin involvement confined to fingers & face. Slow progression.
Late visceral organ involvement. Also with CREST syndrome. More benign clinical course.
Catch with anti-centromere antibodies.

7. Systemic Lupus Erythematosus (SLE) is a chronic systemic “remitting-and-relapsing”

autoimmune disease characterized by several autoantibodies, complement activation, and
immune-complex deposition. It can damage any part of the body.

8. The classic clinical picture of SLE is butterfly (or discoid) rash, polyarthritis, and fever in a
female of reproductive age.

9. Other symptoms of SLE are: photosensitivity, Raynaud phenomenon, alopecia, serositis

(pleuritis/pericarditis), Libman-Sacks endocarditis, cytopenias, oral/nasopharyngeal ulcers, lupus
nephritis, seizures, and psychosis.

10. Diagnosis of SLE is made if the patient meets at least 4 criteria (at least 1 clinical criteria and 1
immunologic criteria) out of 11.

11. Antibodies of SLE are ANA, anti-dsDNA, anti-Sm, antiphospholipid antibodies, and anti-
histone antibodies (in drug-induced lupus).

12. For SLE treatment, oral corticosteroid such as prednisone (15mg or 60mg depending on if
mild/severe) is the mainstay treatment for acute exacerbations. IV methylprednisolone may also
 be used for severe to induce remission in acute exacerbations. For chronic, it’s always
hydroxychloroquine (may cause retinal toxicity).
13. Gout is an acute inflammatory monoarthritis caused by precipitation of monosodium urate
crystals in joints. Most common patients are men over 40 years. The strongest risk factor is
hyperuricemia (due to underexcretion/overproduction), which is over 416 umol/L in men, and
over 360 umol/L in women.

14. Hyperuricemia causes:

- Excessive production (10%): increased turnover of cells; e.g. Lesch-Nyhan syndrome or tumor
lysis syndrome.
- Decreased excretion (90%): renal underexcretion due to CKD or diuretics.

15. In gout, classic manifestation is painful MTP joint of big toe (other common joints are ankles
and knees). Other manifestations of gout are tophus formation (often on external ear, olecranon
bursa, or Achilles tendon). Acute attacks tend to occur after a large meal with foods rich in
purines (e.g. red meat or seafood), trauma, surgery, dehydration, diuretics, or alcohol
consumption.

16. 4 stages of gout:

1. Asymptomatic hyperuricemia.
2. Acute gouty arthritis: sudden onset pain and edema in joints (usually big toe).
3. Intercritical period: asymptomatic period after initial attack (may last 1-2 years).
4. Chronic tophaceous gout: poorly controlled gout w/ tophi; attacks tend to become polyarticular
over time.

17. Diagnosis of gout is by joint aspiration w/ synovial fluid analysis under a polarizing microscope.
See negatively birefringent needle-shaped urate crystals. Blood uric acid levels may be normal
even during an acute attack so not as helpful. Also, do X-ray to see punched-out erosions & tophi.

18. Treatment of acute attacks in gout is NSAIDs (indomethacin), corticosteroids, or colchicine.

Chronic preventive treatment is allopurinol/febuxostat. DO NOT give aspirin, panadol, and
allopurinol during an acute attack.

19. Complications of gout are urate nephrolithiasis, interstitial nephritis, and degenerative
osteoarthritis.

20. Porphyria cutanea tarda is due to uroporphyrinogen decarboxylase defect in liver; exacerbated
with alcohol consumption. Classic symptoms are blistering cutaneous photosensitivity and
hyperpigmentation. Uroporphyrin will be in tea-colored urine. Treatment is phlebotomy,
hydroxychloroquine, and sun avoidance.

21. Porphyria cutanea tarda can be sporadic type (hepatitis C/alcohol) or familial type.
22. Acute intermittent porphyria is due to porphobilinogen deaminase defect in liver, precipitated
by drugs (eg, cytochrome P-450 inducers), alcohol, and starvation.

23. Acute intermittent porphyria’s classic presentation is recurrent abdominal colic, port-wine
urine, tachycardia, and neurological-psychiatric symptoms; PBG & ALA will accumulate in the
dark urine. Treatment is hemin & glucose.

24. Full lipid panel:

Normal total cholesterol: 150-240 mg/dL.
Normal LDL: < 160 mg/dL.
Normal HDL: 30-70 mg/dL.
Normal TAG: < 250 mg/dL.
Ratio of total cholesterol/HDL: < 4.5 is desirable.

25. Familial (primary) dyslipidemias (see the table in ppt):

1. Common primary hyperlipidemia (high LDL only).
2. Familial hypercholesterolemia (absent LDL-receptors in liver; can be heterozygous or homo).
3. Polygenic hypercholesterolemia.
4. LPL deficiency (only triglycerides elevated; pancreatitis is common).
5. Familial combined hyperlipidemia (MC; 1:50; elevated cholesterol + TG).
6. Familial dysbetalipoproteinemia.

26. Atherosclerosis definition: build-up of cholesterol plaques in the intima, leading to thickening
and stiffening of the arterial wall.

27. Complications of atherosclerosis:

- Stenosis due to the large atheroma  ischemia.
- Plaque rupture, leading to thrombus (MI/stroke).
- Plaque rupture, leading to embolus (cholesterol crystals).
- Weakening of vessel wall results in aneurysm (e.g. abdominal aorta).
- Renovascular hypertension.

28. Diagnosis of gastric adenocarcinoma is done via upper endoscopy. Double contrast X-ray is
used for infiltrating carcinomas which spread underneath the mucosa and are not readily visible.

29. Gastric adenocarcinoma must have either subtotal/total gastrectomy, depending on if it’s
proximal or distal. D2 lymph nodes must also be removed.

30. Extraintestinal symptoms of UC are: jaundice (PSC), uveitis, arthritis, and skin lesions
(erythema nodosum or pyoderma gangrenosum).

31. Extraintestinal symptoms of IBD are: uveitis, arthritis, and skin lesions (erythema nodosum or
pyoderma gangrenosum). Additionally, UC can have jaundice (PSC) & toxic megacolon; CD can
 have nephrolithiasis & gallstones.

32. Treatment of UC is sulfasalazine (or mesalamine), may combine with oral corticosteroids. 6-
MU, infliximab, and colectomy (only if debilitating, refractory, and unresponsive to medical
therapy like in toxic megacolon, stricture, severe hemorrhage, and perforation).

33. Treatment of CD is prednisone or budesonide, mesalamine, infliximab, 6-MU/azathioprine,

metronidazole, and surgery (only for complications like strictures, fistulas, perforation, or
abscesses).

34. Both IBD types have risk of malabsorption/malnutrition, colorectal cancer (increased risk with
pancolitis).

35. Benign polyps can be hyperplastic (no malignant potential) or adenomatous (malignant
potential). Adenomatous is further classified into tubular (most common; lowest risk),
tubulovillous, and villous (highest risk).

36. You can determine CRC’s malignant potential by looking at the size (large), histology, atypia,
and shape (sessile & flat are more likely malignant vs pedunculated on a stalk).

37. Polyps are found usually in the rectosigmoid area, and are usually asymptomatic completely;
they will bleed, if anything. Polyps look very similar to cancers so they ALL need to be
completely removed & biopsied.

38. Colonoscopy is the diagnostic test of choice for symptomatic diverticulosis. CT abdomen and
pelvis with IV contrast (check renal parameters) is best initial step for diverticulitis, and then do
colonoscopy 6-8 weeks after the acute episode to assess the extent of the diverticulitis and rule
out malignancy.

39. Classes of malabsorption disorders: digestion, absorption, secretion, motility.

40. Types of gallstones: cholesterol (90%) & pigment (black is caused by hemolysis and cirrhosis;
brown is caused by infection).

41. Gallstones are caused by:

1. Supersaturation of cholesterol or bilirubin.
2. Decreased bile acids.
3. Biliary stasis.

42. Asymptomatic gallstones aren’t operated on; painful/complicated stones are operated on.

43. If a bile stone is obstructed in the cystic duct, it will cause biliary colic. Eventually it will stay in
the cystic duct long enough to develop inflammation and turn into acute cholecystitis, and the
 pain becomes constant, with fever + leukocytosis. In this case, NG suction, NPO, IV fluids, and
antibiotics “cool down” most cases, allowing elective cholecystectomy to follow 6 weeks later.

44. If the stone reaches the common bile duct, it causes partial obstruction and ascending infection,
becoming acute ascending cholangitis (far more deadly and septic). Fever will spike, very high
WBCs, and possibly sepsis. Extremely high ALP and high bilirubin. Give IV antibiotics + IV
fluids + emergency decompression of the common bile duct via ERCP to save the patient’s life.
Removal of stone via ERCP and sphincterotomy; may put a stent. Cholecystectomy must be done
soon after.

45. Charcot triad of acute ascending cholangitis: RUQ pain + jaundice + fever. Reynolds pentad:
triad + septic shock + altered mental status. Hepatic abscess is the most serious complication.

46. Murphy’s sign is gallbladder pain at the RUQ during inspiration. It is positive in cholecystitis.

47. Acute viral hepatitis (HAV, HEV, or HBV) clinical picture occurs usually in 3 stages:
prodromal (1-2 weeks), icteric (1-3 weeks), and convalescence (1-3 months). Few patients
progress to acute liver failure. Diagnosis is with LFTs & serology (IgM antibody against HepA);
treatment is supportive; vaccine exists (both pre- and post-exposure).

48. Other causes of acute hepatitis are: autoimmune, paracetamol, amanitin, and alcohol.

49. Look for HBsAg and IgM anti-HBc antibodies to diagnose hepatitis B infection.

50. In the HBV prodromal phase, rash, arthritis, and fever may arise. Extrahepatic manifestations of
HBV are polyarteritis nodosa & membranous glomerulonephritis.

51. Chronic hepatitis may be caused by HBV, HCV, autoimmune hepatitis, alcohol, paracetamol,
and NAFLD.

52. Jaundice is not very typical for chronic hepatitis; it is more common in the acute form.

53. In chronic hepatitis, liver biopsy is useful for grading (activity of inflammation) and staging
(degree of fibrosis).

54. Manifestation of cirrhosis:

1. Lowered detoxification capability: hepatic encephalopathy, jaundice, gynecomastia, spider
angioma, palmar erythema.
2. Decreased synthetic function: coagulopathy (bleeding), hypoproteinemia (edema),
immunodeficiency (no antibodies  infection!).
3. Portal hypertension: ascites, varices, splenomegaly (hypersplenism  thrombocytopenia),
edema.
55. An HVPG (hepatic venous pressure gradient) of ≥ 5 mmHg defines portal hypertension, and if
the measurement exceeds 10 mmHg it is called clinically significant portal hypertension. Above
12 mm Hg, variceal hemorrhage may occur.

56. TIPS (transjugular intrahepatic porto-caval shunt) is a good cure for portal hypertension!
Basically, a shunt is created between the higher-pressure portal vein and the lower-pressure
hepatic vein.

57. For esophageal varices treatment, first treat the shock/blood loss (if any) with IV fluids, IV
antibiotics prophylactically (IV ceftriaxone), start IV octreotide for 3-5 days, then do endoscopic
band ligation or injection sclerotherapy. Prevention is with propranolol or TIPS.

58. Definition of acute liver failure is INR over 1.5 + hepatic encephalopathy + no previous liver
disease (usually < 26 weeks).

59. Complications of acute liver failure are infection, cerebral edema (elevated ICP), hepatic
encephalopathy, and hemorrhage.

60. Benign liver tumors are hepatic adenoma, cavernous hemangioma (MC), and focal nodular
hyperplasia. Generally all asymptomatic, but large tumors may cause pressure/fullness/pain.
There is risk of rupture! Diagnose using US, and then CT scan. Please discontinue OCPs. Surgery
only in large tumors over 5 cm.

61. General diagnosis of vasculitis includes: CRP/ESR, CBC (leukocytosis), antibodies (e.g.
ANCA, IgA in Henoch-Schonlein, and IgE in Churg-Strauss), biopsy (w/ IF), and angiography.

62. Every male patient with UTI is considered to have “complicated UTI”.

63. For diagnosis of UTI, first do urine dipstick and check leukocyte esterase & nitrites. Significant
bacteriuria defined as ≥ 105 CFU/mL confirms a UTI on urine culture.

64. RPGN is divided into 3 classes: anti-GBM, ANCA, and immunocomplex.

65. Chronic GN causes: IgA nephropathy (MC), membranous nephropathy, MCD, FSGS, and
MPGN.

66. Acute tubulointerstitial nephritis = allergies (e.g. rash) + AKI (e.g. oliguria). Usually caused
particularly by antibiotics and NSAIDs that act as haptens, inducing a hypersensitivity reaction.
Eosinophils will be in urine and blood, along with hematuria and slight proteinuria. Can also be
caused by infection.

67. Chronic tubulointerstitial nephritis = renal papillary necrosis eventually leads to fibrotization
of the interstitium and atrophy of tubules, presenting as gross hematuria and flank pain. Etiology
 is analgesic nephropathy (e.g. NSAIDs or paracetamol) or infection/multiple myeloma. Usually
leads to CKD eventually.

68. Chronic pyelonephritis is interstitial fibrosis and atrophy of tubules due to multiple bouts of
acute pyelonephritis. Usually there is VUR or BPH/cervical carcinoma or some other obstruction.
Must be targeted abx therapy.

69. AD PCKD is when macrocysts press on the kidney parenchyma, destroying it. It’s related to
berry aneurysms and liver cysts. Presents in young adults as flank pain, HTN (due to increased
renin), hematuria, and worsening renal failure, leading to CKD. Furthermore, the cysts may
become infected.

70. CKD is defined as either decreased kidney function (eGFR <60 mL/min) or kidney damage
(proven by albuminuria > 30 mg/day) for at least 3 months, regardless of cause. Diabetes and
hypertension are the 2 most common causes of ESRD. Chronic GN is 3rd. Other causes are
pyelonephritis and PCKD.

71. For CKD staging, GFR is divided into grades 1-5 (CKD is grade 3, CRF is grade 5); albuminuria
is divided into grades 1-3. eGFR is calculated with [serum Cr] using MDRD formula.

72. For AKI, learn RIFLE criteria. For CKD, learn KDOQI.

73. Normal creatinine is 60-120 umol/L; normal urea is 2.5-8.0 mmol/L.

74. Main cause of death in CKD patients is HF due to volume overload, and then infections.

75. For respiratory acidosis diagnosis, normal pCO2 is 4.5-6.0 kPa. If pCO2 and HCO3- go
opposite directions, it’s a mixed disorder.

76. Metabolic alkalosis can be divided into:

- Dehydration (low ECF/low urine chloride): vomiting & diuretics. These respond to normal
saline. Also, correct the hypokalemia with KCl 7.5%.
- Hyperhydration (high ECF/high urine chloride): usually hyperaldosteronism due to adrenal
adenoma/hyperplasia. These are resistant to normal saline.

77. Most common cause of respiratory acidosis is COPD (hypoventilation). On the other hand,
respiratory alkalosis is caused by any hyperventilation (including high altitude and anxiety).

78. Dehydration types:

- Isoosmolar: bleeding, burns, diarrhea, edema.
- Hypoosmolar: aldosterone deficiency (Addison’s disease), diuretics, oliguric phase of AKI.
- Hyperosmolar: sweating, osmotic polyuria (DM), DI, and low water intake.
79. In renal causes of dehydration, always check urine sodium, which will be low (< 20 mmol/L) in
case it’s a renal problem.

80. Dehydration treatment:

- Frequent monitoring of HR, BP, urine output, and weight is essential.
- Isoosmolar: normal saline.
- Hypoosmolar: 3% NaCl solution with 7.5% KCl.
- Hyperosmolar: 5% glucose solution.
- Adult maintenance fluid: D5 1/2NS + 20 mEq/L KCl. Dextrose is added to inhibit muscle.
- Maintain urine output at 0.5-1 mL/kg/hr.
- If very ill, consider placing a Swan–Ganz catheter (to measure CVP and PCWP).

81. If you bring sodium down low too fast  brain edema (must not be faster than 0.5 mmol/L/hr). If
you increase it up high too fast  central pontine myelinolysis (must not be faster than 1.0
mmol/L/hr).

82. The symptom of hyponatremia is brain edema (increased ICP, seizures, coma)!

83. Hyperkalemia = over 5.2 mmol/L (do dialysis if over 7).

Hypokalemia = below 3.5 mmol/L.

84. Hyperkalemia treatment: calcium gluconate + insulin/glucose + B2 agonist + HCO3 + diuretics

(+ dialysis).

85. Hypokalemia treatment: first correct Mg, then 7.5% KCl.

86. Transplantation:
- Kidneys: indicated in CKD stage 5; may be preserved for 24-36 hours; heterotopic method;
inserted into right iliac fossa.
- Liver: indicated in Child-Pugh score B-C; may be preserved for 12 hours; orthotopic method.
- Heart: indicated in NYHA 3-4 or EF < 20% or if drugs don’t work or predicted survival < 1
year; may be preserved for 6 hours; bicaval orthotopic method.
- Lungs: indicated in terminal stages of diseases which have no drug alternatives remaining
(COPD, CF, bronchiectasis, IPF, pulmonary HTN); check lung allocation score; may be
preserved for 6 hours; bilateral transverse transsternal thoracotomy most common.

87. HPSC transplant:

- Auto-transplant indicated in myeloma, lymphoma and AML.
- Allogenic transplant indicated in AML, ALL, aplastic anemia, MDS, sickle, thalassemia,
immunodeficiency.
- Can be taken from bone marrow, peripheral blood after prior stimulation, or umbilical cord
blood.
- First take the HPSCs, then do myeloablation, then IV infusion of the HPSCs back into the body.
 - Immunosuppression required for allogenic transplant because of risk of GvHD.

88. Functional geriatric exam includes:

- Health status (full history with targeted questions like vision, hearing, incontinence, balance,
malnutrition, and vaccinations).
- Physical performance & self-sufficiency (ADL/IADL).
- Mental function (MMSE).
- Social status (family and housing situation).

89. Pharmacokinetics in geriatric patients is different because they have prolonged half-life,
slower elimination, decreased absorption (slower onset), and lower distribution.

90. In geriatric patients, start with a low dose. Wait for the effect, and only if necessary, increase it
slowly (start low-go slow). E.g. omeprazole or statins require half doses in the elderly.

91. Pericarditis treatment is with NSAIDs and colchicine.

92. Myocarditis shows a clinical picture of HF, and is treated as such.

93. For Tuberculosis, know the epidemiology of Czechia because Marel may ask about it. Also, the
patient will be subfebrile only; no high fever.

94. For AKI, we use the RIFLE criteria. For CKD, we use KDOQI criteria + albuminuria levels.

95. PSGN may occur with strep pharyngitis or skin infection. Rheumatic fever only occurs with
strep pharyngitis.

96. First-line treatment for osteoporosis is bisphosphonates (alendronate). Second line is SERMS
(raloxifene).

97. Pancreatitis is most commonly due to alcohol & gallstones.

98. n/a

99. Good luck