MRCP Part 2 Flashcards

Question

AML - what is on blood film

Answer 1

Blast cells with auer rods

Answer 2

deletion chromosome 5 (5q-)

Answer 3

>11 = Cirrhosis w/ portal htn, budd-chiari, RHF <11 TB peritonitis, nephrotic syndrome (low albumin), malignancy/pancreatitis

Answer 4

1. Aspirin 300mg two weeks 2. Clopi 75 mg + simsvastatin thereafter

Answer 5

transabdominal USS + CA125

Answer 6

electromyography

Answer 7

Membranoproliferative glomerulonephritis

Answer 8

lymphocytic infiltration of colon, associated w/ chron's/ibd, and setraline use --> diarrhea dx colonic biopsy (lymphocitic infiltration) management - withdraw agent and loperamide, cholestyramine

Answer 9

intraperitoneal vancomycin and gentamycin as coagulase -ve staphylococcus is common organism

Answer 10

PREGNANCY! CARBAMAZAPINE = CYP450 Inducer = reduces COCP => pregnancy

Answer 11

=renal atherosclerosis , rx = angioplasty

Answer 12

Quinine / Quinidine (Class 1A antiarrythmic - sodium channel blocker slows rapid depolarisation during phase 0) => vomiting, vertigo, tinnitus, headache and blurry vision

Answer 13

polyarteritis nodosa 1) small-medium sized vasculitis 2) purpura, livido reticularis 3) hep b 4) microaneurysms renal artery 5) mononeuritis multiplex (foot drop), 6) transient visual loss 7) c and p-anca -ve 8) esr raised 9) corticosteroids + cyclophosphamide

Answer 14

1) concave ST elevation - saddle shaped 2) PR depression II , V6 3) PR elevation aVR

Answer 15

1) Forced vital capacity (FVC) is the maximum amount of air you can exhale after inhaling fully 2) 3.0-5 L 3) in GBS - FVC = best measure of prognosis

Answer 16

1. Klebsiella pneumoniae 2. Pneumonia + Lung abscess (cavitation) 3. 3rd gen cephalosporins (ceftriaxone) quinolones e.g levofloxacin

Answer 17

1) direct coombs + mycoplasma serology 2) macrolides (clarithromycin) mycoplasma

Answer 18

1. recurrent fever 2. peritonitis (severe abdo pain) 3. pericarditis, pleuritis, synovitis (arthralgias w/ clear fluid aspiration) 4. attacks lasting 24-72 hours 5. rx = colcichine

Answer 19

degeneration of myenteric plexus

Answer 20

1. >20% blast cells in BM or <20% if specific clonal abnormalities seen 2. cloncal abnormalities t(8:21)(q22;q22), inv(16)(p13;q22), t(16;16)(p13;q22), t(15:17)(q22;q12) 3. monocytoid cells with auer rods

Answer 21

1. carbimazole 2. discontinue amiodarone 3. prednisolone 4. discontinue amiodarone (long half life so controversial 58 days)

Answer 22

1) seminomatous germ cell tumours - bhcg (with hyperthyroid sx - due to b-hcg acting on thyroid gland - similar structure to tsh, same alpha subunit and similar beta subunit) 2) non-seminomatous germ cell tumours - afp

Answer 23

1) peripheral eosinophilia 2) veil like upper lobe collapse , or pulmonary infiltrates 3) causes - asthma 4) dx rast/ igG a. fumigatus, raised IgE>1000

Answer 24

1) dried - gabepentin/pain relief 2) oral aciclovir 3) iv aciclovir

Answer 25

reduce platelet function so increase risk of bleeding

Answer 26

presynaptic alpha 2 adrenoceptor antagonist (increases serotonergic and noradrenergic neurotransmission)

Answer 27

1) protease inhibitor 2) nephrolithasis 3) urine crystals

Answer 28

1. =levofloxacin or macrolides 2. doxycycline

Answer 29

oral itraconazole

Answer 30

microangiopathic haemolytic anaemia (ldh increase, reticuloycytosis, bilirubin rise, low hb), thrombocytopenia neurological abnormalities fever renal dysfunction rx = ffp, methylpred, plasma exchange CI = platelet transfusion cause = adamts13 deficiency (can't cleave platelets so they clot)

Answer 31

stop fondaparineux only if can (as clopi and aspirin stop stent thrombosis)

Answer 32

1. s.a 2. pseudomonas aeruginosa

Answer 33

ring enhancing lesions (1/2) sulfadiazine + pyrimethamine + folinic acid + dexamethasone

Answer 34

cryptococcal meningitis (lymphocytosis , low glucose, raised opening pressure, raised protein ) in csf - in hiv

Answer 35

hiv - jc virus

Answer 36

modafinil (cns stimulant)

Answer 37

CMV colitis (Rx gangiciclovir)

Answer 38

Anticholingeric

Answer 39

1) metoprolol (Metoprolol doesn't shorten the QT but reduces arrhythmia risk by blunting sympathetic triggers, blocks b1 receptors, Blocks β1-adrenergic receptors → ↓ sympathetic drive Reduces heart rate and myocardial excitability Stabilizes the cardiac action potential Prevents sudden surges of catecholamines that can trigger torsades) 2) ICD 3) left cervicothoracic stellectomy

Answer 40

vit b12 (reduced absorption)

Answer 41

blocks inhibitory NT glycine and GABA

Answer 42

splenomegaly, anaemia, thrombocytopenia, monocytopenia abnormal b-lymphocytes with eccentric nuclei / abnormal villous projections rx purine analogues cladribine, pentostatin

Answer 43

blocks acetycholine => paralysis

Answer 44

b) radio/chemotherapy because peri-operative risk is high of stroke

Answer 45

neutrophils (neutrophilic dermatosis)

Answer 46

Sweet syndrome is a skin disease that causes a sudden rash, fever, and high white blood cell count. It's also known as acute febrile neutrophilic dermatosis.

Answer 47

growth hormone

Answer 48

ICU input for noradrenaline infusion to maintain an adequate BP

Answer 49

1) Autosomal dominant 2) hamartomas (A hamartoma is a non-cancerous growth that's made up of an abnormal mixture of cells. Hamartomas can occur in many parts of the body, including the brain, skin, mouth, and gastrointestinal tract), sclerotic fibromas (on skin), trichilemommas (skin-coloured wart like strucutres) 3) breast ca, thyroid mass/malignancy, colorectal cancer, macrocephaly

Answer 50

abstinence from alcohol

Answer 51

farm worker (bacteria Brucella abortus zoonotic disease) -->back pain, constipation, pyrexia of unknown origin, hepatosplenomegaly, unsteady gait, generalised hypotonia

Answer 52

Treatment - IVF, bromocriptine/dantrolene

Answer 53

Dantrolene depresses excitation-contraction coupling in skeletal muscle by binding to the ryanodine receptor 1, and decreasing intracellular calcium concentration

Answer 54

dopamine agonist

Answer 55

thrombocytopenia, purpura (vasculitis - inflammed blood vessels leak into skin), arthritis, abdo pain, haematuria complication - glomerulonephritis

Answer 56

Calcium Oxolate (short bowel syndrome) - most common - Chron's , resected short bowel, increased oxolate permeability , which is absorbed and excreted in excess therefore, rx calcium citrate supplementation hydration and reduced oxolate.. Calcium Phosphate Uric Acid (Gout) Struvite (Proteus) Cystine (Cystinuria)

Answer 57

Parrafin containing emollients

Answer 58

Glioblastoma multiforme Rx gross total resection , radiotherapy and chemo (temozolamide - oral alkylating agent)

Answer 59

Strep bovis Bacteriodes Rx metronidazole

Answer 60

Renal vein thrombosis / AKI (hypercoaguable state due to loss of protein c , s , and antithrombin 3)

Answer 61

IV lignocaine (unless significant cardiovasciular instability, or IV phenytoin class IB antiarrhythmic properties (like lidocaine). It can be used to treat ventricular arrhythmias, especially: Digoxin-induced ventricular tachycardia or ventricular ectopy. Blocks voltage-gated sodium channels (fast Na⁺ channels). Shortens the action potential duration in ischemic or depolarized myocardial tissue. Suppresses abnormal automaticity and stabilizes cardiac membranes. First-line = Digoxin-specific antibody fragments (Digibind). Phenytoin or lidocaine can be used to control the arrhythmias if needed urgently. then give synochronised DC cardioversion

Answer 62

obstruction of intrahepatic veins - can be a complication of behcets abdo pain, ascites, and jaundice (portal hypertension)

Answer 63

sulphonylurea abuse (increased endogenous insulin production) => hypoglycemia

Answer 64

1. parasitic rx - nitazoxanide 2. supportive 3. rx HIV underlying

Answer 65

1. spiculated margins 2. distortion of neighbouring vessels with spiculated margins 3. ground-glass shadowing 4. cavitation/pseudo cavitation

Answer 66

1) cavitation - gas filled space within nodule, mass or area of consolidation due to necrosed lung tissue 2) pseudocaviation - resemeble cavitaties but are dilated bronchioles or small cysts (air/fluid filled)- can be due to adenocarcinoma, emphysema

Answer 67

1) n. gonorrhea 2) Im ceftriaxone

Answer 68

improved diet - take 60 mins before eating to prevent motor - on/off symptoms (as its absorbed in duodenum) as dietary proteins can compete for its absorption and transport in gi system and to bbb reducing its effects

Answer 69

kallman - hypogonadotropic hypogonadism (low LH) klinefelter - 47xyy - primary hypogonadism (raised LH)

Answer 70

iv glucocorticoids

Answer 71

1) nrti 2) dilated cardiomyopathy 3) lipodystrophy on bloods (high tg for example)/insulin resistance

Answer 72

motor only, assymetric weakness, LMN signs, GM1 antibodies (anti-ganglioside) rx IVIG

Answer 73

staphylococcus epidermidis/aureus rx - vancomycin for staph epidermidis (coagulase -ve and resistant to penicillin)

Answer 74

small papula initially then ulcerates, spread by sandflies (parasitic disease rx sodium stibogluconate

Answer 75

fever, weight loss, hepatosplenomegaly --> anaemia and fatigue, rx liposomal amphotericin B

Answer 76

ABPA - Aspergillus total serum IgE and IgG precipitins towards Aspergillus Fumigatus CEP - Raised total IgG, asthma peripheral infilitrates, simlar to ABPA, rx steroids

Answer 77

pseudomonas aurgineousa, staph aureus diabetic and I.C

Answer 78

consider encephalitis (change personality, neuro signs) and myocolonus and rapidly progressing dementia investigations - CSF analysis for 14.3.3 protein and RTQuIC, eeg MRI - signal changes in putamen and head of caudateN

Answer 79

high LDH and uric acid (tumor lysis), over days/weeks - very rapid doubling time (25H)

Answer 80

neovascularisation of the iris rx - panretinal photocoagulation, anti-vegf

Answer 81

AR -> progressive LMN weakness , then later bulbar weakness (pneumonia/resp failure) , parents first cousins type 1 = onset before 6 months type 3 = child to adolsecent, less sever

Answer 82

due to lupus anticoagulant binding phospholipids in lab tests

Answer 83

viral - non-bloody often (norovirus, rotavirus, enteric adenovirus, astrovirus) bacterial - bloody often (most common - c. jejuni, salmonella , shigella)

Answer 84

worse headache in morning, b/l papilledema, cranial neuropathy ix - cranial imaigng (CT, MRI), r/o SoL

Answer 85

low vit d secondary to cancer (e.g. CLL) - malignancy produces FGF23 --> reduced 1,25 dihydroxy vit d by kidneys and phosphate reabsorpation --> low phosphate (rickets, osteomalacia), rx - vit d and phosphate supplements

Answer 86

IV tazocin or oral fluoroquinolones

Answer 87

hookworm - Necator americanus , ancylostoma duodenale rx - albendazole, mebendazole

Answer 88

1) seconds to minutes episodes of worst headache 2) multisegmental cerebral artery vasoconstriction 3) pseudoephirene (vasoconstrictor), triptans, 4) rx - management bp - labetalol, ccb

Answer 89

multi-layers compression banding

Answer 90

mantoux test can be -ve

Answer 91

reduce dose amlodipine when starting clari, macrolides inhibit cyp3a4 (amlodipine metabolised by cyp3a4) => increase vasodilatory effect/renal injury

Answer 92

Bartter = Like loop diuretics (blocks NKCC2) → hypercalciuria Gitelman = Like thiazide diuretics → hypocalciuria + hypomagnesemia, but presents later than barters Liddle = Looks like hyperaldosteronism but aldosterone is low all are inherited renal tubulopathies ----- All have hypokalemia + metabolic alkalosis 1) Bartter - NKCC2 inhibiton (Na⁺/K⁺/2Cl⁻) thick ascending limb LOH, hypercalciuria, sodium loss, normal/low bp, increased AR, autosomal recessive 2) Gitelman - NCC inhibition (Na⁺/Cl⁻ co-transporter (NCC), DCT, hypocalciuria, sodium loss, normal/low bp, -low magnesium, increased AR, autosomal recessive 3) Liddle - ENaC- gain of function, sodium reabsorption, htn in youth, normal Mg, normal calcium, reduced AR, Autosomal dominant

Answer 93

1) Tropheryma whipplei (a gram-positive actinomycete) + Immune response - multisystem but GI predominant 2) CAN MALA C- Chronic diarrhea, abdo pain, fever A- Arthralgia N- Neurological (dementia, myoclonus, ataxia, etc.) MALA - Malabsorption (steatorrhea, WL, anameia) 3) dx - jejunal biopsy- macrophages + for Periodic acid schiff staining , HLAB27 4) rx lt abx that cross bbb Initial IV antibiotics (to penetrate CNS): Ceftriaxone or penicillin G for 2–4 weeks Followed by long-term oral therapy (to prevent relapse): Trimethoprim-sulfamethoxazole (TMP-SMX) for 12 months

Answer 94

rounded opacity surrounding by halo of air similar px to tb - wl, haemoptysis

Answer 95

thrombocytosis, thrombocytopenia, anemia, raised esr

Answer 96

in chinese remedies, hypokalemia, htn, metabolic alkalosis, normal r:a

Answer 97

Renin ↑ High Aldosterone ↑ High RAR Normal or ↓ Low

Answer 98

1) Haemoglobin made from haem + globin --> haem made from protoporhyrin 9 and Fe2+. Porphyria is AD due to defect in porphobillinogen deaminase, required to make up protoporphyrin 9 --> toxic porphyrin precursors triggered by stressors (drugs-sulphonamides, baributrates, ocp, anti-epileptics), fasting, alcohol, hormones (attack in luteal phase due to increased progesterone) 2) 4 P's Pain - abdo pain (w/o peritonitis) Psych - anxiety,hallucination, agitation Peripheral - Peripheral neuropathy Pink/Purple Urine (on standing urine becomes darker tdue to porphyrins) 3) PBG increased in attack, ALA, urine and faecal porphyrins, 4) IV hemin (feedback inhibition of ALA synthase) High-dose glucose (inhibits ALA synthase) ALA is neurotoxic and leads to symptoms

Answer 99

iv fluids, supporitve

Answer 100

1) RVH , RAD, P pulmonale 2) Pul artery pressure via RH catheterisation >25 mmHg 3) PDE-5 Inhibitors - sildefanil endothelin receptor blocker - bosentan prostacyclin analgoues (PGI2) - iloprost CCB - if +ve vasodilator test = first choice.

Answer 101

Acute vasoreactivity testing (AVT) is a key diagnostic step during right heart catheterization in patients with pulmonary arterial hypertension (PAH) to identify those who might benefit from calcium channel blockers (CCBs). if mPAP drop >10 mmHG if not then can go to targetted pul htn therapies

Answer 102

Hereditary hemorrhagic telangiectasia (HHT) – telangiectasia , autosomal dominant, AVMs in lungs, GI, brain (Haemorrhage)

Answer 103

1) extrinsic allergic alveolitis (type of ILD) 2) hypersensistivity pneumonitis due to inhaler avian proteins in feathres (IgA) 3) reduced tlco, reduced kco, 4) corticosteroids, avoid allergen

Answer 104

farmers lung - Micropolyspora faeni, thermatinomyces in hay,straw,grain malt workers - aspergiullus clavatus

Answer 105

UL needs sun care (SST CARE) SST CARE S – Silicosis S – Sarcoidosis T – Tuberculosis C – Coal Workers’ Pneumoconiosis A – Ankylosing Spondylitis R – Radiation E – Extrinsic Allergic Alveolitis (EAA) aka Hypersensitivity Pneumonitis

Answer 106

steroids (topical/oral)

Answer 107

beta blockers, vinblastine, bleomycin, ocp, ergotamine

Answer 108

SSZ, leflunomide, AZA but mostly SSZ

Answer 109

1) unconjugated gilberts syndrome , criggler najjar (ugt1a1 gene defect => udp glucuronyl transferase) deficiencies 2) conjugated - transport deficiencies) dubin-johnson (MRP2 def) (dark granules within hepatocytes) rotor (OATP def) (normal liver histology)

Answer 110

aspirate + 10 days metronidazole

Answer 111

AION - ischemia of optic nerve head - supplied by posterior ciliary arteries - e.g. secondary to vasculitis/GCA CRAO - pale fundus with cherry red spot at macula , no disc swelling (embolic/thrombic) both painless monocular vision loss

Answer 112

1) topical/oral steroids 2) iv infliximab

Answer 113

1) renal biopsy, low urine, low osmolality, ur:cr <40 2) abx (pen, ceph), nsaids, allopurinol 3) conservative unless uremic

Answer 114

T1-ASMa T2-A-LKM T3 -Soluble Liver-Kidney Ag all have gamma-globulin ag raised all respond to steroids

Answer 115

1) muscle glycogen phosphorylase deficiency => inability to breakdown glycogen in muscle =>accumulation of glycogen and early fatige 2) second wind when switch to aerobic respiration using glucose frmo blood 3) no raised lactate (deficient glycogen/glucose to lactate) 4) Possible myoglobinuria (cola-colored urine) after strenuous activity → risk of acute kidney injury the enzyme deficiency limits ATP generation by glycogenolysis and results in glycogen accumulation Treatment for muscle phosphorylase deficiency consists of preexercise consumption of simple carbohydrates (e.g., sucrose or sports drinks) to protect muscles and improve exercise tolerance prior to the onset of the second wind

Answer 116

acute sarcoidosis erythema nodosum, bhlad, joint sx

Answer 117

eosinophils in lungs due to parastitic infection (ascarisis lumbricoides)

Answer 118

pneumoconiosis + RA => rheumatoid nodules in lungs Pneumoconiosis refers to a group of interstitial lung diseases caused by inhalation of inorganic dusts, leading to chronic lung inflammation and fibrosis.

Answer 119

1. Liver Disease Leads to Increased Vasodilators In cirrhosis or portal hypertension, the liver fails to clear vasodilatory substances (especially nitric oxide). This causes systemic and pulmonary vasodilation. 2. Intrapulmonary Vascular Dilations (IPVDs) Pulmonary vessels, especially at the bases, become abnormally dilated. Capillaries widen → oxygen molecules can't efficiently diffuse across the increased distance → impaired oxygenation. 3. Ventilation-Perfusion (V/Q) Mismatch Blood flows through dilated vessels too quickly, and/or too far from alveoli, causing inadequate oxygen exchange. Also contributes to a right-to-left intrapulmonary shunt (blood bypasses oxygenation). 4. Result: Hypoxemia Arterial blood has low oxygen content despite normal or increased ventilation. Positional hypoxia (worsens when upright) = platypnea–orthodeoxia syndrome Platypnea = Shortness of breath that worsens on sitting or standing (opposite of usual cases) Orthodeoxia = Drop in oxygen saturation when moving from lying down to standing Intrapulmonary vascular dilatations (IPVDs) are more prominent in the lung bases (due to gravity and regional blood flow). When you stand up: Blood is redistributed more toward the lower zones of the lungs. These dilated vessels act like a shunt — blood flows through them without getting properly oxygenated. More blood flows through poorly oxygenated areas, leading to worsening hypoxemia. When lying down (supine): Blood flow is more evenly distributed throughout the lungs. Less shunting → better oxygenation Treatment is with oxygen supplementation and liver transplantation

Answer 120

beta blockers

Answer 121

cranial di - post desmopressin test urine osmolality >660 , little to no response in nephrogenic diabetes insipidus

Answer 122

intranasal desmopressin

Answer 123

stop offending agent or hypokalemia/hyperca bendroflumethiazide

Answer 124

granuloma with prominent epitheloid cells with sparse lymphocytic infiltrate at the margins

Answer 125

Corticobasal degeneration

Answer 126

1) AR 2) calcified microliths in alveolar space

Answer 127

in sample tube for lt or secondary to essential thrombocytosis => hyperkalemia => in tube lysis

Answer 128

PT>100 (most sensitive) serum cr >300 arterial ph < 7.3 INR>6.5 grade 3 or 4 hepatic encephalopathy

Answer 129

p.v - flaccid and mucous membranes b.p - tense blisters rx - steroids

Answer 130

gram negative coccobaccilus macrolides only useful if used in first 3 weeks

Answer 131

ischemic colitis (represent thickening of the colonic haustral folds and are a sign of severe submucosal edema)

Answer 132

1) stop smoking to stop COPD, PPI, nintedanib, pirfenidone, pul rehab to improve symptoms PPI improves survival time

Answer 133

When given with other antiemetics (additive effect)

Answer 134

HSV encephalitis

Answer 135

Prolonged QTc and flat t waves

Answer 136

when at 6 month surveillance low grade dysplasia doesnt resolve with high dose PPI

Answer 137

1) S.A 2) p. Aeruginosa

Answer 138

1. Pseudomonas Aeruginosa 2. Klebsiella Pneumoniae 3. MRSA rx- piperacillin tazobactam

Answer 139

cytoalbuminogenic dissociation -gbs

Answer 140

1. diptheria antitoxin + erythromycin

Answer 141

if woken up with symptoms - no thrombolysis/thrombectomy just give aspirin 300mg

Answer 142

think anti-gbm disease (as alports = abs to collagen t4) => rpgn w/o pulmonary haemorrhage

Answer 143

leucoerythroblastic anemia myelofibrosis, cml, myeloma, malignant marrow infiltration, polycythemia rubra vera, sarcoidosis, tb of bone marrow, osteopetrosis

Answer 144

dysuria -> neutrophil on penile swab no organisms on microscopy due to ureaplasma urealyticum, mycoplasma genitalum rx doxycycline *first line or azithromycin if allergic

Answer 145

hypokalemia hypocalcemia hyperphosphatemia hyperuricaemia AKI raised LDH give allopurinol to prevent it (inhibit xanthine oxidase prevents uric acid formation) rx- rasburicase (converts uric acid to allantoin in established TLS - more soluble) ivf , correct electrolytes ?dialysis

Answer 146

1. peritoneal carcinomatosis (tumour cells infiltrate peritoneum - disrupt normal fluid absorption and leak protein fluid into peritonealcavity) 2. obstruct lymphatic drainage (cant reabsorb peritoneal fluid) 3. increased capillary permeability (cytokines increase vascular permeability - relased by tumours) 4. portal hypertension (e.g. hepatic mets or primary liver ca) 5. hypoalbuminaemia (due to cytokine release - supressing hepatic albumin production = negative acute-phase reactant, liver dysfunction, increased cap permeability, protein losing enteropathy - direct damage to gi mucosa, malnutrition & cahcexia)

Answer 147

because not enough iron - give it IV (w/o iron cant build haemoglobin in RBCs!!) oral poorly absorbed

Answer 148

1) S4 (stiff LV) 2) Ejection systolic murmur left lower sternal border - doesn't radiate to carotids 3) Valsalva - decreasaes preload (less venous return -> worse obstruction of LV outflow tract) =>murmur louder 4) Squatting - increases preload and afterload, more blood in heart increasing chamber size pushing hypertrophied septum out the way/reducing LV outflow tract) = quieter murmur 5) AD mutations in sarcomere - b myosin heavy chain (MYH7 gene) and myosin binding protein c (MYBPC3 gene)=> myocyte hypertrophy, disarray, and fibrosis + assymetric septal hypertrophy (LVOT) anterior mitral valve pulled towards septum during systole (sysolic anterior motion => dynamic obstruction) => mitral regurg + diastolic dysfunction (impaired relaxtion and filling) => elevated lv end diastolic pressure => pul congetsion and dyspnea, thickened myocardium => more o2 req => angina with normal coronaries arrythmias due to fibrosis/myocyte disarray (AF, VT,SCD)

Answer 149

inability of lv to contract forcefully (dilated cardiomyopathy) unlike s4 = hypertrophic cardiomyopathy also due to htn , aoritc regurg

Answer 150

1) gluten free diet 2) dapsone 3) sulfapyridine

Answer 151

1-alpha hydroxylase

Answer 152

1) sodium nitroprusside stored in sunlight/polyurethrane burning 2) hypertension, bradycardia, then hypotension and coma 3) rx sodium thiosulphate, dicobalt edetate, sodium nitrate (any)

Answer 153

12-16 mmhg Pul Art 2-6 mmHg R atria 8-10 mmHg (L atria) Pul artery wedge 15-30 R ventr

Answer 154

thrombophilic disorders

Answer 155

both are natural anticoagulants, that bind and inactivate factor v and factor 8 factor v leiden - unable to respond to protein c and cant inactivate factor v

Answer 156

carcinoid syndrome - do ct chest and abdo

Answer 157

5 HIAA urinary Plasma CgA Seurm seratonin CT to look for primary

Answer 158

after patients with MRI in ckd patients get gadolinium contrast --> they develop symptoms of systemic sclerosis, autoabs all negative

Answer 159

does not fit into any single category -serositis, pul febrisosi, pericarditis, sclerodactylyl etc. anti-rnp postive almost always

Answer 160

small l apical pneumothorax if pa and AP cxr normal consider lateral decubitus

Answer 161

e.g. in leg post-procedure (cholesterol dislodged) - angiography/stenting/carotid endarterectomies/initiating warfarin AKI, eosoinophilia, distal limb rash livido reticularis Eosinophilia is part of the immune response to the cholesterol emboli. Livedo reticularis is caused by microvascular obstruction and impaired circulation due to emboli. AKI results from vascular obstruction and ischemia in the kidneys caused by the cholesterol crystals lodging in renal vasculature.

Answer 162

1) Acute Mountain Sickness (AMS), High altitude pulmonary edema (HAPE), High altitude cerebral edema (HACE) 2) AMS - headache, N&V, HAPE - cyanosis, chest pain, rapid breathing, HACE - confusion, headache 3) AMS - acetazolamide, HAPE - o2, nifedipine, HACE - dex, o2 all need descent acetazolamide - causes intracellular acidosis , shifts o2 dissociation curve to right = so low PP - more o2 to tissues AMS: Hypoxia-induced vasodilation in the brain, cerebral edema, and altered neurological function. HAPE: Pulmonary vasoconstriction, excessive fluid leakage into alveoli, and impaired gas exchange. rx 100% o2 HACE: Cerebral vasodilation and increased blood-brain barrier permeability leading to cerebral edema and increased intracranial pressure.

Answer 163

Beta-2 Microgloblin (increased tumour burden, renal failure)

Answer 164

1) ancylostoma duodenale, necator americanus 2) via feet 3) intense local rash then to lungs where cause wheeze and cough then migrate to intestine, become adult and leave eggs => abdo pain, diarrhea, anaemia 4) 8-12 weeks see hookworm eggs in stools 5) anthelminthic drugs - mebendazole, albendazole, thiabendazole , ivermectin

Answer 165

bromocriptine, carbegoline (DA's)

Answer 166

x axis pO2 (mmHg) Y-axis % saturation hb with o2 S shaped curve at higher o2 saturations , hb almost fully saturated and lower o2 saturations, hb less saturated R shift = decreased affinity of hb for o2, more to tissues causes = CADET, face Right! → ↑ CO₂, ↑ Acid (H⁺) = (↓ pH), DPG (2,3-BPG), Exercise, Temperature ↑ HbF = increased affinitiy of hb for o2 ↓ CO₂, ↓ H⁺ (↑ pH), ↓ temp, ↓ 2,3-BPG, CO poisoning, fetal Hb Left-shifted curve: helps fetus extract O₂ from maternal blood CO greater affinity of Hb than O2 by 200x (l ward shift)

Answer 167

2,3-Diphosphoglycerate (2,3-DPG) is produced in red blood cells via a side pathway of glycolysis (the Rapoport-Luebering shunt). It binds to deoxygenated hemoglobin and reduces its affinity for oxygen → facilitates O₂ release to tissues. Decreases 2,3-DPG — “SAFE blood” holds oxygen tight Reduces oxygen delivery to tissues (left shift). Promotes oxygen unloading to tissues. HATCHET Hypoxia – triggers 2,3-DPG to help release more O₂ to low-oxygen tissues Altitude (high) – low atmospheric O₂ → compensatory increase in 2,3-DPG Thyrotoxicosis – increased metabolism drives glycolysis and 2,3-DPG production Chronic anemia – fewer RBCs → body increases 2,3-DPG to maximize O₂ delivery Heat (elevated temperature) – speeds up metabolism and glycolytic activity Exercise – increased oxygen demand boosts 2,3-DPG for tissue delivery Talks alkalosis (↑ pH) – alkalotic conditions enhance 2,3-DPG synthesis SAFE Stored blood – 2,3-DPG degrades over time, reducing O₂ release capacity Acidosis – acidic conditions inhibit enzymes that produce 2,3-DPG Fetal hemoglobin (HbF) – naturally has low affinity for 2,3-DPG → higher O₂ affinity Electrolyte issue: Hypophosphatemia – phosphate is needed for 2,3-DPG synthesis2

Answer 168

Mycobacterium avium intracellulare, CD4 count<50

Answer 169

Large infarct, cardioembolic stroke, thrombolysis, anticoagulants, hypertension, hyperglycaemia, old age, early reperfusion, poor collaterals, BBB disruption, thrombocytopenia, and high NIHSS score. Mnemonic: “CHART HOP BLEED” C - Cardioembolic stroke H - Hyperglycaemia A - Anticoagulants R - Reperfusion (early) T - Thrombolysis (tPA) H - Hypertension O - Old age P - Poor collaterals B - BBB disruption L - Large infarct E - Elevated NIHSS score E - Endothelial injury D - Decreased platelets

Answer 170

patients no longer at risk of MALT lymphoma

Answer 171

anti-acetylcholine receptor abs repetive nerve stimulation/single fibre emg tensilon test

Answer 172

chlorhexidine but needs hospital

Answer 173

primary lymphedema, yellow nails, recurrent pleural effusions Impaired or malformed lymphatic vessels → ↓ lymph drainage Leads to: Peripheral lymphedema Pleural effusions Sinus and respiratory tract congestion Also affects nail matrix → yellow discoloration, thickening, and slow growth

Answer 174

1) TPHA/FTA-ABS Detect T. pallidum-specific antibodies, used for confirmation, stay positive for life. 2) VDRL/RPR Detect antibodies to host lipids, used for screening & monitoring, false positives from viral infections, pregnancy, autoimmune disease. False positives: Non-treponemal = "V-PRAISE Me" (viral, pregnancy, RA, autoimmune, IVDU, SLE, elderly); Treponemal = rare, sometimes autoimmune or cross-reactivity. Treponomal = if negative = no syphilis, if positive move to RPR RPR = positive in active syphilis , can be used to monitor treatment. + T + RPR = active syphilis + T - RPR = past syphilis or latent - T - RPR = No syphilis - T + RPR = FP “P-VIRAL” mnemonic: Pregnancy Viral infections (HIV, hepatitis) IV drug use Rheumatic/autoimmune (e.g., SLE, RA) Ageing Leprosy / Malaria / TB

Answer 175

Yaws is a chronic skin, bone, and cartilage infection caused by: Treponema pallidum pertenue Endemic in tropical rural regions: Africa, Asia, South America, Pacific Islands Direct skin-to-skin contact with infectious lesions No insect vector, no sexual contact involved single dose iv ben pen Primary Yaws: Starts with a painless papule (called “mother yaw”) that ulcerates and crusts. Secondary Yaws: Multiple skin lesions appear (papules, nodules, ulcers), often with bone pain and swelling. Common bones affected: Tibia, fingers, and toes — periostitis is typical. Other features: Lymphadenopathy, mild fever, and malaise may occur. Tertiary Yaws (rare): Causes deep ulcers, bone destruction, nasal deformities (goundou), and facial disfigurement. No CNS or heart involvement (unlike syphilis).

Answer 176

Sinus tachycardia Transient atrioventricular (AV) block Atrial fibrillation Transient AV block Atrial flutter Transient AV block Atrioventricular nodal re-entrant tachycardia (AVNRT) May terminate Atrioventricular re-entrant tachycardia (AVRT) May terminate Ventricular tachycardia Likely to have no effect

Answer 177

aflut = reentrant circuit in RA, regular (unless variable block) = rx with ablation afib = multifocal disorganized electrical impulses, irregularly irregular = rate/rhythm ctrl, anticoag

Answer 178

macrolides, ciprofloxacin, cimetidine, allopurinol, ocp rx in asthmatics svt = verapamil

Answer 179

levetiracetam

Answer 180

4-12 na+-hco3-cl

Answer 181

Mnemonic – HARDASS H – Hyperalimentation (TPN) A – Acetazolamide R – Renal tubular acidosis (RTA) - R = renal tubular acidosis (Type I = distal; Type II = proximal; Type IV = hyporeninemic hypoaldosteronism. D – Diarrhoea A – Addison’s disease S – Spironolactone S – Saline infusion (0.9% NaCl) F - fistula (URETEROENTEROSTOMY)

Answer 182

1) post-lateral infarct involving av node 2) monitor (3% after MI) and self-resolves

Answer 183

Renal Tubular Acidosis (RTA) – Summary of All 4 Types RTA refers to a group of disorders characterized by a normal anion gap (hyperchloremic) metabolic acidosis, due to defects in renal acid handling. low bicarb, low ph Type 1 – Distal RTA Defect: Impaired hydrogen ion (H⁺) secretion in the distal tubule. Urine pH: Greater than 5.5 (urine remains alkaline despite systemic acidosis). Serum Potassium: Low (hypokalemia). Complications: Kidney stones (nephrolithiasis), nephrocalcinosis, bone demineralization. Causes: Autoimmune diseases (e.g., Sjögren’s syndrome), hereditary forms, drugs (e.g., amphotericin B), hypercalciuria. Type 2 – Proximal RTA Defect: Impaired bicarbonate (HCO₃⁻) reabsorption in the proximal tubule. Urine pH: Initially above 5.5, later falls below 5.5 as bicarbonate levels drop. Serum Potassium: Low (hypokalemia). Associated with: Fanconi syndrome (generalized proximal tubule dysfunction). Causes: Multiple myeloma, certain medications (e.g., acetazolamide), inherited disorders (e.g., cystinosis). Type 3 – Mixed RTA (Obsolete) Definition: Previously considered a combination of Type 1 and Type 2 features. Current Status: No longer commonly used as a separate category. Seen in: Rare inherited disorders, such as carbonic anhydrase II deficiency (may cause both proximal and distal defects). Type 4 – Hyperkalemic RTA Defect: Decreased aldosterone effect → impaired sodium reabsorption and reduced H⁺ and K⁺ secretion in the distal tubule. Urine pH: Typically below 5.5 (can vary). Serum Potassium: High (hyperkalemia). Common in: Diabetic nephropathy, chronic kidney disease, patients on RAAS inhibitors. Causes: Hypoaldosteronism (e.g., Addison’s disease), ACE inhibitors, ARBs, NSAIDs, potassium-sparing diuretics (e.g., spironolactone). Quick Mnemonic Type 1 – Problem with acid excretion (distal tubule). Type 2 – Problem with bicarbonate reabsorption (proximal tubule). Type 4 – Aldosterone issue, leads to hyperkalemia. + HTN

Answer 184

radiotherapy HL

Answer 185

1) defect in calcium-sensing receptor (CaSR) on parathyroid glands and kidneys (GPCR) CaSR normally suppresses PTH when serum calcium is high. In FHH, the mutated CaSR underestimates calcium levels, thinking they’re lower than they actually are. Result: PTH secretion is inappropriately normal or mildly elevated, despite hypercalcemia. -- The renal CaSR also thinks calcium is low, so it reduces urinary calcium excretion. This leads to hypocalciuria (low calcium in urine), a hallmark of FHH. so dif with primary hyperparathyroid: both: high/normal PTH, high serum ca, but FHH - low Ca in urine

Answer 186

1) Normal to Mildly Low Magnesium → Stimulates PTH Magnesium is essential for normal PTH secretion. If magnesium drops slightly, the body perceives it like hypocalcemia: ➜ Stimulates PTH secretion. ➜ Increases renal calcium reabsorption, bone resorption, and vitamin D activation. 2) Severe Hypomagnesemia → Suppresses PTH At very low Mg²⁺ levels, magnesium is required for: Synthesis, secretion, and action of PTH. Without it: ➜ PTH secretion fails, even if calcium is dangerously low. ➜ Target tissues also become resistant to PTH. Result: A paradoxical situation: Hypocalcemia Low or inappropriately normal PTH This can mimic hypoparathyroidism! --- Mechanisms Involved: Magnesium acts intracellularly to allow cAMP generation and PTH exocytosis. Also affects CaSR sensitivity—though less than calcium itself.

Answer 187

localised scleroderma 20-40 year old - waxy /pale skin absent hair and sweating, provoked by trauma or infection rx local steroids, phototherapy

Answer 188

hypersensitivity reaction to schistosoma larvae and eggs - mansoni/japonicum - swimming in endemic waters (2-8 weeks post infection) - (like Sub-Saharan Africa, South America, parts of Asia). fever, myalgia, headache, itchy rash increased eosinophils cxr increased vascular and interstitital markings rx praziquantel, corticosteroids

Answer 189

neutropenia splenomegaly RA rx CS/cyclophosphamide

Answer 190

diurnal variation in cortisol levels remain (higher in morning, 50% of that at night) due to chronic alcohol abuse/depression True Cushing’s = endogenous, pathological hypercortisolism Pseudo-Cushing’s = reversible activation of HPA axis due to another underlying condition

Answer 191

45X webbed neck, gonadal dysgenesis (primary amenorrhea, tall, wide-spaced nipples), absent ovaries, slow secondary characteristics dx - elevated lh/fsh, rx- combined estrogen/progesterone

Answer 192

1) Pathophysiology: Zenker’s diverticulum is a pharyngoesophageal (hypopharyngeal) false diverticulum It forms through Killian's dehiscence: A weak area between the thyropharyngeus and cricopharyngeus muscles (both part of the inferior pharyngeal constrictor) It’s a false diverticulum: only mucosa and submucosa herniate through the muscle wall Caused by: Impaired relaxation or spasm of the cricopharyngeal muscle during swallowing This ↑ intraluminal pressure → outpouching of mucosa posteriorly 😬 2) Symptoms: Often insidious and progressive: Dysphagia (especially to solids, progressing to liquids) Regurgitation of undigested food (may occur hours after eating) Halitosis (bad breath from trapped food) Cough, aspiration, hoarseness Gurgling in the neck or a palpable neck mass In severe cases: weight loss, aspiration pneumonia 🔍 3) Investigations: Barium swallow (gold standard): Reveals a posterior outpouching at the pharyngoesophageal junction Confirms size, location Endoscopy: Done carefully (risk of perforation) Useful pre-op or for ruling out malignancy (rare) CXR: May show air-fluid level if large Avoid endoscopy as first-line unless needed, due to perforation risk 💊 4) Treatment (Rx): 🩺 Asymptomatic/small (<1–2 cm): Often observe (no intervention if no impact) 💉 Symptomatic or large diverticula: Surgical/endoscopic options: Endoscopic stapling or laser diverticulotomy (minimally invasive) Preferred in many cases now Divides the cricopharyngeal muscle and opens the pouch Open surgical excision (diverticulectomy) with cricopharyngeal myotomy Done if endoscopy

Answer 193

ABCDE" causes of Long QT" A – Antiarrhythmics (Class Ia & III: Amiodarone, Sotalol, Quinidine, Procainamide) B – Antibiotics (esp. macrolides like erythromycin, and fluoroquinolones like ciprofloxacin) C – CNS drugs (e.g., antipsychotics, TCAs, SSRIs-citalopram,escitalopram, lithium) D – Diuretics (due to electrolyte disturbances – ↓ K⁺, Mg²⁺, Ca²⁺) E – Electrolyte imbalances (↓ K⁺, Mg²⁺, Ca²⁺)

Answer 194

<20 years old need to do renal USS again, as false negatives

Answer 195

distal to subclavian systolic murmur/continuous murmur epistaxis htn radio-femoral delay cold peripheries intermittent claudication

Answer 196

Cinacalcet binds allosterically to the CaSR (calcium-sensing receptor) This makes the receptor more sensitive to circulating calcium So, even normal or low calcium levels are now “interpreted” as high This leads to reduced PTH secretion Ultimately causes: ↓ Parathyroid hormone (PTH) ↓ Serum calcium ↓ Serum phosphate (indirectly) used in Secondary hyperparathyroidism in CKD (especially on dialysis) Primary hyperparathyroidism in patients not fit for surgery Parathyroid carcinoma with hypercalcemia

Answer 197

V1-V3 st elevation + RBBB (SC5NA) cardiac arrythmia- abnormal sodium depolarisation (gene codes for sodium channels) - no structural abnormalities, pure electrical abnormalities of myocardial cells

Answer 198

caused by mutations affecting the mitochondria young adult - myoclonus, myopathy, exercise intolerance, short stature, unexplained diabetes optic atrophy csf lactic acid and csf pyruvic acid

Answer 199

benign myoclonic epilepsy of infants

Answer 200

AST:ALT 2:1 Chronic alcohol use leads to vitamin B6 (pyridoxal phosphate) deficiency. ALT is more dependent on B6 than AST. As a result, ALT activity drops, contributing to the elevated AST:ALT ratio. and also ALT only in cytosol, ast in mitochondria and cytosol, alcohol induces both mitochondrial and cytosol damage Also, the enzyme elevations tend to be modest (rarely over 300–500 IU/L) compared to viral or ischemic hepatitis.

Answer 201

ct abdo, lipase

Answer 202

Infarct of lateral medulla due to PICA or vertebral artery occlusion. Don't PICA WALLs with SAD Horn" Dysphagia, hoarseness (Nucleus ambiguus - CN IX, X) → Ipsilateral Pain/temp loss face (Spinal trigeminal nucleus) → Ipsilateral Weakness of pain/temp body (Spinothalamic tract) → Contralateral Spinocerebellar tract (Ataxia) → Ipsilateral Ataxia + Dizziness (Vestibular nuclei) → Ipsilateral Horner's syndrome (Sympathetic fibers) → Ipsilateral ✅ Face = Ipsilateral, Body sensation = Contralateral. Lateral Medullary Ipsilateral CN IX, X, V Contralateral pain/temp body

Answer 203

Infarct of midbrain (anterior) due to paramedian branches of PCA. WeB = Weak Body + Blown pupil" Weakness of body (Corticospinal tract) → Contralateral Lower facial droop/dysarthria (Corticobulbar tract) → Contralateral Blown pupil, ptosis, "down and out" eye (CN III palsy) → Ipsilateral ✅ Motor weakness = Contralateral, Cranial nerve III = Ipsilateral. Weber Ipsilateral CN III Contralateral motor weakness

Answer 204

allopurinol because its a xanthine oxidase inhibitor (XO = Reduce uric acid production by inhibiting xanthine oxidase, the enzyme that converts hypoxanthine → xanthine → uric acid.) XO also metabolises 6-MP -> toxic levels 6-MP

Answer 205

due to hep c infection (blood screening started then)

Answer 206

1) Vector: Triatomine bugs ("kissing bugs") 2) Investigations: Acute phase: Blood smear for trypomastigotes Chronic phase: Serology (anti-T. cruzi IgG) PCR (highly sensitive, early detection) ECG (arrhythmias, conduction blocks) Echo (cardiomyopathy, ventricular aneurysms) Barium swallow if esophageal involvement (megaesophagus) 3) Symptoms: Acute Phase: Fever, malaise Romaña sign: unilateral painless periorbital edema Hepatosplenomegaly Lymphadenopathy Chronic Phase (years later): Dilated cardiomyopathy, heart failure Arrhythmias, sudden cardiac death Megaesophagus (dysphagia, regurgitation) Megacolon (severe constipation) 4) Treatment: Acute phase: Benznidazole (first-line) Nifurtimox (alternative) Chronic phase: Antiparasitic treatment still offered early Manage organ damage (heart failure meds, pacemaker, surgery)

Answer 207

1) aedes mosquite 2) Sudden high fever Severe headache, retro-orbital pain Myalgia ("breakbone fever") Arthralgia Rash (diffuse maculopapular) Bleeding tendencies: petechiae, epistaxis, gum bleeding Severe dengue: Plasma leakage → shock, respiratory distress, organ failure 3)Supportive care (mainstay!) Fluid resuscitation (critical in severe cases) Acetaminophen for fever (avoid NSAIDs → bleeding risk) 4) NS1 antigen test (early, day 0–5) Dengue IgM/IgG serology (after day 5) PCR (if available, early phase) CBC: Thrombocytopenia, leukopenia Elevated hematocrit (plasma leakage in severe dengue) LFTs: Elevated AST/ALT CXR/Ultrasound: Pleural effusions, ascites (severe cases)

Answer 208

dmd at younger age bmd at older age (20 or so) and milder sx

Answer 209

hsv encephalitis

Answer 210

funny channel inhibitor In heart failure, the heart is already weak and struggling to pump. ➔ A high heart rate increases myocardial oxygen demand and shortens diastole (the filling phase), making things worse. Ivabradine slows the heart rate without reducing contractility. ➔ More time for diastolic filling ➔ better stroke volume. ➔ Less oxygen demand on already stressed heart muscle. By optimizing heart rate (usually targeting ~60 bpm): ➔ Improves cardiac efficiency ➔ Reduces hospitalizations and improves symptoms in HFrEF patients.

Answer 211

direct thrombin inhibitor

Answer 212

Heparin binds to Antithrombin III (ATIII). This binding causes a conformational change in ATIII, greatly accelerating its ability to inactivate clotting factors — mainly: Thrombin (Factor IIa) Factor Xa Result: Prevents conversion of fibrinogen to fibrin, stopping clot formation

Answer 213

OS - Center of atrial septum (fossa ovalis) Incomplete fusion of septum primum + secundum Most common ASD (~70%) Left → right (usually) Isolated, or with MVP, migraine, etc. May close spontaneously or via catheter/surgery if large Wide, fixed split of S2 + soft systolic ejection murmur (pulmonary flow murmur) - Left-to-right shunt → increased flow across pulmonary valve - Incomplete right bundle branch block (RBBB) (rSR' in V1) - Right axis deviation OP - Lower part of atrial septum (near AV valves) Failure of septum primum to fuse with endocardial cushions Left → right (usually) shunt AV septal defects, Down syndrome surgical Wide, fixed split of S2 + holosystolic murmur (tricuspid regurgitation) - Left-to-right shunt + defective AV septum → tricuspid regurg - Left axis deviation - First-degree AV block (prolonged PR interval) Defect near AV node → conduction delay and altered depolarization PFO - Fossa ovalis (like OS ASD) Foramen ovale remains functionally open, but not a true septal defect Usually closed Paradoxical emboli, cryptogenic stroke, migraine with aura no rx no murmur at rest unless valsalva Usually normal ECG Ix - all Echo with bubble study or color Doppler

Answer 214

1. Right heart volume overload In ASD, left-to-right shunt → increased blood flow to the right atrium and right ventricle. The right ventricle dilates and stretches because it handles excess blood volume. 2. Conduction system stretching The dilation of the right ventricle stretches the conduction fibers (specifically the right bundle branch). Stretching delays the electrical impulse traveling down the right bundle. 3. Why incomplete RBBB, not complete? The conduction delay is mild to moderate (not a total block). So you see an rSR' pattern in V1: r = small initial positive deflection (normal septal depolarization) S = negative deflection R' = delayed right ventricular depolarization However, QRS duration stays <120 ms, which defines it as incomplete RBBB (if >120 ms → complete RBBB).

Answer 215

1. Left-to-Right Shunt → Right Heart Volume Overload In OS ASD, blood shunts from the left atrium to the right atrium. This leads to chronic volume overload of the right atrium and right ventricle. 2. Right Ventricular Enlargement Over time, the right ventricle dilates and hypertrophies to handle the extra volume. A bigger, hypertrophied right ventricle has more electrical mass. 3. Shift in Electrical Vector Since the right ventricle is enlarged, the main electrical depolarization vector shifts rightward. On ECG, this shows up as Right Axis Deviation (RAD). Defect location Ostium primum ASD is low in the atrial septum, close to the atrioventricular (AV) valves and the AV conduction system. It disrupts the normal development of the AV septum, including tissues that guide electrical conduction. 2. Abnormal conduction through the ventricles Instead of normal fast conduction, the electrical impulse detours abnormally through displaced conduction pathways. This delayed activation of the right ventricle and preferential conduction on the left side pulls the axis leftward. 3. Associated valve abnormalities OP ASD is often associated with cleft mitral valve or AV canal defects, leading to altered ventricular geometry and further leftward conduction shift.

Answer 216

gpa (haematuria, haemoptysis + systemic vasculitis) Cytoplasmic (diffuse cytoplasm) - PR3 antigen p-anca perinuclear antigens -MPO Microscopic Polyangiitis (MPA) Eosinophilic Granulomatosis with Polyangiitis (EGPA, Churg-Strauss) Others: IBD, primary sclerosing cholangitis c-ANCA (PR3) = think nosebleeds, sinus destruction, cavitating lung nodules (GPA) p-ANCA (MPO) = think pulmonary hemorrhage + glomerulonephritis (MPA) without classic ENT features.

Answer 217

SICKFACES.COM — CYP3A4 Inhibitors (Inhibitors slow down metabolism → ↑ drug levels--> increased warfarin --> increased INR) Mnemonic: 👉 SICKFACES.COM Letter Drug S Sodium valproate I Isoniazid C Cimetidine K Ketoconazole F Fluconazole A Alcohol (acute use) C Chloramphenicol E Erythromycin (and other macrolides) S Sulfonamides . (dot = spacer) C Ciprofloxacin O Omeprazole M Metronidazole

Answer 218

CRAP GPS — CYP3A4 Inducers (Inducers speed up metabolism → ↓ drug levels--> dcerase warfarin -->decrease INR) Mnemonic: 👉 CRAP GPS Letter Drug C Carbamazepine R Rifampin A Alcohol (chronic use) P Phenytoin G Griseofulvin P Phenobarbital S St. John's Wort

Answer 219

"HOCM = H-LAQ-T" Hypertrophy (LVH) - Tall R waves in V5–V6, deep S waves in V1–V2 Left atrial enlargement - Broad/notched P waves (especially in lead II) Arrhythmias - Possible atrial fibrillation, ventricular ectopics Q waves (pseudo-infarct) - Deep, narrow "pseudo-infarct" Q waves (inferior and lateral leads) T wave inversions - Especially in anterolateral leads (V4–V6) ST segment depression or T wave changes VT _ Seen in severe cases — risk for sudden death The deep, narrow Q waves can mimic old MI — but they’re due to septal hypertrophy, not infarction. If a young patient has syncope + LVH + abnormal ECG, always think of HOCM. ECG may be normal in ~10% early cases!

Answer 220

(Hypergastrinemia = Elevated gastrin levels in the blood) Zollinger-Ellison Syndrome (Gastrinoma) - Gastrin-secreting tumor (pancreas or duodenum) → massive acid hypersecretion Hypochlorhydria / Achlorhydria (low/no stomach acid) Chronic atrophic gastritis Pernicious anemia Less acid → feedback to secrete more gastrin Proton pump inhibitors (PPIs) - Blocking acid secretion → compensatory ↑ gastrin Helicobacter pylori infection - Alters antral regulation of gastrin secretion Gastric outlet obstruction -Gastrin accumulates due to poor gastric emptying GAP HP" for Hypergastrinemia: Gastrinoma (Zollinger-Ellison) Atrophic gastritis / Achlorhydria PPIs Helicobacter pylori Physical blockage (outlet obstruction) Gastrinoma: Very high gastrin + acidic pH. Atrophic gastritis/pernicious anemia: High gastrin + alkaline pH (because no acid is produced). Situation Response to Secretin Why Normal G-cells ↓ Decrease gastrin Secretin inhibits gastrin normally Gastrinoma ↑ Increase gastrin Secretin paradoxically stimulates tumor cells Always interpret secretin test along with gastric pH: Low gastric pH (<2) + high gastrin + positive secretin test = classic for gastrinoma.

Answer 221

1. Normal physiology: Secretin is released by the duodenum in response to acid in the small intestine. It normally inhibits gastrin release from normal G-cells in the stomach. Secretin also stimulates bicarbonate secretion from the pancreas to neutralize acid. 2. What happens in Gastrinoma cells: Gastrinoma cells (tumor cells) are abnormal — they express secretin receptors that are miswired. Instead of inhibiting gastrin secretion, secretin stimulates these tumor cells to secrete even more gastrin. 3. Mechanism: Secretin binds to abnormal receptors → activates cAMP pathway → increases gastrin secretion instead of suppressing it.

Answer 222

Pernicious anemia is a type of macrocytic anemia caused by vitamin B12 deficiency due to autoimmune destruction of gastric parietal cells. (Auto abs) It results in loss of intrinsic factor, which is needed to absorb vitamin B12 in the ileum Autoantibodies against parietal cells or intrinsic factor --> Gastric atrophy (chronic atrophic gastritis) --> Loss of intrinsic factor Poor vitamin B12 absorption Vitamin B12 deficiency --> Impaired DNA synthesis → macrocytic anemia

Answer 223

A rare neurological condition where a patient is cortically blind (due to bilateral occipital lobe damage) but denies their blindness and confabulates (makes up explanations). (e.g. AF) Bilateral occipital lobe damage (primary visual cortex). Disconnection between visual processing and conscious awareness. Damage also affects parts of the brain that provide insight into deficits (like frontal-parietal networks), leading to anosognosia. Anosognosia is a neurological condition where a patient is unaware of or denies a disability or deficit (even though it's obvious to others).

Answer 224

Severe liver dysfunction (e.g., cirrhosis) leads to portal hypertension and systemic vasodilation, especially in the splanchnic circulation (gut blood vessels) 🔹 Trigger: Advanced liver disease (e.g., cirrhosis) Portal hypertension and splanchnic vasodilation occur. 🔹 Pathophysiology Steps: Splanchnic vasodilation → pooling of blood in the gut vessels → ↓ effective arterial blood volume. Kidneys sense decreased perfusion pressure ("perceived hypovolemia"). Activation of vasoconstrictor systems: ↑ RAAS, ↑ sympathetic nervous system, ↑ ADH. Intense renal vasoconstriction to maintain blood pressure. Severe ↓ renal blood flow → ↓ GFR → renal failure, despite structurally normal kidneys. Kidneys are structurally normal — the dysfunction is functional. Does not fully respond to volume resuscitation (unlike simple hypovolemia). Potentially reversible with liver transplant. 🔹 Types: Type 1 HRS: Rapid, severe renal failure. Type 2 HRS: Slower progression, often associated with refractory ascites. HRS = Kidney shutdown → need vasoconstrictors + albumin. HPS = Lung blood vessels dilate → need oxygen and transplant.

Answer 225

plasma cell infiltration of salivary and lacrimal glands (anti-ro anti-la), positive schirmers test rx artifical tears, opthalmic assessment for corneal ulceration and dryness and dental carries

Answer 226

🔹 MEN 1 ("3 Ps") Mnemonic: 👉 "MEN 1 = 3 P's" Parathyroid hyperplasia (→ hypercalcemia) Pituitary tumors (e.g., prolactinoma) Pancreatic neuroendocrine tumors (e.g., gastrinoma, insulinoma) ✅ Mutation: MEN1 gene (menin protein, tumor suppressor) 🔹 MEN 2A ("2 P's + 1 M") Mnemonic: 👉 "MEN 2A = 2 P's and 1 M" Parathyroid hyperplasia (less common than MEN1) Pheochromocytoma Medullary thyroid carcinoma (MTC) ✅ Mutation: RET proto-oncogene (gain-of-function) 🔹 MEN 2B ("1 P + 2 M's") Mnemonic: 👉 "MEN 2B = 1 P and 2 M's" Pheochromocytoma Medullary thyroid carcinoma (more aggressive than 2A) Mucosal neuromas (plus Marfanoid habitus) ✅ Mutation: RET proto-oncogene (different point mutation from MEN 2A)

Answer 227

AD disease that leads to retinal and CNS tumours including phaeochromocytoma, renal cysts, cerebellar haemangioblastoma HTN, balance issues, headaches, dizziness Why does polycythemia happen in VHL? In VHL syndrome, patients can develop renal cell carcinomas (especially clear cell type) or hemangioblastomas (particularly in the cerebellum and spinal cord). These tumors can produce excess erythropoietin (EPO). EPO stimulates the bone marrow to produce more red blood cells → secondary polycythemia. hemeangioblastomas If you see a young patient with a cystic cerebellar mass and secondary polycythemia, think VHL-associated hemangioblastoma.

Answer 228

Histoplasmosis is a fungal infection caused by Histoplasma capsulatum Inhalation of spores from contaminated soil, especially: Bird or bat droppings (e.g., caves, chicken coops, old buildings). Clinical Manifestations: Asymptomatic in most healthy people. Acute pulmonary histoplasmosis: fever, cough, chest pain, flu-like symptoms; may mimic pneumonia. Chronic pulmonary histoplasmosis: seen in COPD patients, resembles tuberculosis with cavitary lung lesions. Disseminated histoplasmosis: occurs mainly in immunocompromised patients (e.g., HIV/AIDS), leading to hepatosplenomegaly, bone marrow suppression (pancytopenia), oral ulcers, and adrenal involvement. Serology (histoplasma antibodies). Mild to moderate disease: usually self-limiting; may use itraconazole if needed. Severe or disseminated disease: start with amphotericin B, then switch to itraconazole for maintenance therapy. "Histoplasmosis Hits the Histocytes" — Histoplasma lives inside macrophages (histiocytes). bilateral adrenal swelling -> do groccot-stained biopsy

Answer 229

benzylpenicillin + cloindamycin

Answer 230

What is urinary alkalinization? It means making the urine more alkaline (higher pH), usually by giving IV sodium bicarbonate. Rhabdomyolysis-induced AKI Muscle breakdown releases myoglobin. Myoglobin can precipitate in acidic urine, forming casts and causing direct tubular toxicity. Alkaline urine reduces myoglobin precipitation and neutralizes free radicals. Tumor lysis syndrome (TLS) Massive cell death releases uric acid. Uric acid is more soluble in alkaline urine, reducing risk of uric acid crystal nephropathy. Use urinary alkalinization carefully — it’s not for all AKI types. Monitor potassium closely: bicarbonate can shift potassium into cells and cause hypokalemia.

Answer 231

Alport’s syndrome consists of: Nephritis – causing microscopic haematuria and progressive kidney disease with episodic frank haematuria Ocular pathology – corneal ulcerations, bilateral anterior lenticonus, bilateral dot-fleck marks around the fovea Progressive high-frequency sensorineuronal deafness

Answer 232

iv ciclosporine

Answer 233

In hepatic encephalopathy, lactulose works mainly by reducing the amount of ammonia in the blood. Here’s the mechanism in simple steps: Lactulose is a non-absorbable sugar that reaches the colon undigested. In the colon, gut bacteria ferment lactulose into lactic acid and acetic acid, which acidifies the colon. The more acidic environment converts ammonia (NH₃) into ammonium (NH₄⁺). Ammonium is charged and can't easily cross cell membranes, so it stays trapped in the gut and gets excreted in stool. Lactulose also speeds up gut motility, which reduces the time for ammonia to be absorbed. So overall: less ammonia gets into the blood → less toxicity to the brain → improved encephalopathy. 2) Rifaximin works by killing ammonia-producing bacteria in the gut. More precisely: It’s a poorly absorbed antibiotic that stays in the intestines. It targets gut bacteria that make ammonia and other toxins. With fewer bad bacteria, less ammonia is produced and absorbed into the blood. This helps prevent or treat hepatic encephalopathy.

Answer 234

IV artesunate

Answer 235

dimercaptosuccinic acid

Answer 236

phase 1&2 often combined

Answer 237

A VIPoma is a rare neuroendocrine tumor that secretes excess vasoactive intestinal peptide (VIP). VIP causes massive watery diarrhea, leading to dehydration, hypokalaemia (low potassium), and achlorhydria (low stomach acid). This classic triad is remembered as WDHA syndrome: ➔ Watery Diarrhea, Hypokalaemia, Achlorhydria. Most VIPomas arise in the pancreas (especially the tail). Diagnosis involves finding high plasma VIP levels and often imaging (CT, MRI) to localize the tumor. Treatment usually involves surgical removal; octreotide (a somatostatin analogue) can help control symptoms before surgery. raised plasma chromografin A "Chromogranin A is a blood marker for detecting neuroendocrine tumors, but can be falsely raised by PPIs."

Answer 238

albendazole tip: stop carbemazapine as reduces drug availability

Answer 239

form of cutaneous sarcoidosis characterized by red to purple or violaceous indurated plaques and nodules, primarily affecting the nose, cheeks, ears, and lips rx steroids

Answer 240

acrokeratosis paraneoplastica (psoriasis type erythametous scaly rash), indigestio/food sticking, nail dystrophy

Answer 241

"Carotid sinus hypersensitivity causes syncope via exaggerated vagal activation (bradycardia) and/or sympathetic withdrawal (hypotension) in response to minor neck stimulation." The carotid sinus detects blood pressure changes through baroreceptors. In hypersensitivity, minor stimuli (like turning the head, shaving, tight collars) trigger an exaggerated reflex. This reflex causes: Increased vagal tone → bradycardia (slow heart rate). Peripheral vasodilation via sympathetic withdrawal → hypotension (low blood pressure). Result: Syncope (fainting) or near-syncope due to reduced cerebral blood flow. There are 3 types: Cardioinhibitory (mainly bradycardia or asystole) Vasodepressor (mainly hypotension) Mixed (both bradycardia and hypotension)

Answer 242

budesonide - find intraepitheleal lymphocytes and subepitheleal collagen deposits

Answer 243

Central obesity (increased waist circumference) High blood pressure (≥130/85 mmHg or on treatment) High fasting glucose (≥5.6 mmol/L or diagnosed diabetes) High triglycerides (≥1.7 mmol/L) Low HDL cholesterol ("good cholesterol") Men: <1.0 mmol/L Women: <1.3 mmol/L

Answer 244

Mitotane is an adrenolytic drug — it destroys adrenal cortex cells. Main use: It’s used to treat adrenocortical carcinoma (a rare adrenal gland cancer). Sometimes also used for Cushing’s syndrome if surgery isn’t an option. Mechanism: Inhibits steroidogenesis (blocks cortisol and other adrenal steroid production). Directly toxic to adrenal cortex cells → causes adrenal atrophy over time.

Answer 245

Nephrotic syndrome = massive proteinuria (>3.5g/day) + hypoalbuminaemia + oedema + hyperlipidaemia. Minimal change disease (most common in children; can be triggered by infections, NSAIDs) Focal segmental glomerulosclerosis (FSGS) (common in adults; linked to HIV, obesity, heroin use) Membranous nephropathy - membraneous glomerulonephritis - IgG and C3 deposition (common in adults; associated with cancer, hepatitis B/C, autoimmune disease) Secondary (systemic diseases affecting the kidney) Diabetes mellitus (diabetic nephropathy — most common cause overall) Systemic lupus erythematosus (SLE) Amyloidosis Infections (e.g., hepatitis B, hepatitis C, HIV, malaria) Drugs (e.g., NSAIDs, gold, penicillamine)

Answer 246

IgA nephropahty / buergers disease - glomerulonephritis IgA Nephropathy (Berger’s Disease) ➔ Typically causes a nephritic syndrome, NOT nephrotic. Main feature: recurrent visible haematuria, especially after infections (like a sore throat). Sometimes can cause mild proteinuria, but haematuria dominates. Rapidly Progressive Glomerulonephritis (RPGN) ➔ Also nephritic, NOT nephrotic. Characterized by rapid loss of renal function over days to weeks. Microscopy shows crescents in glomeruli (crescentic GN). Causes include: Goodpasture’s syndrome (anti-GBM antibodies) ANCA-associated vasculitis (GPA, MPA) Severe post-infectious GN

Answer 247

Nephrotic Massive proteinuria, oedema, hypoalbuminaemia, hyperlipidaemia Nephritic Haematuria (blood in urine), hypertension, oliguria, mild/moderate proteinuria, active urinary sediment (RBC casts) Nephrotic syndrome is caused by diseases like Minimal Change Disease, Focal Segmental Glomerulosclerosis (FSGS), Membranous Nephropathy, Diabetic Nephropathy, and Amyloidosis, all of which lead to massive protein loss, hypoalbuminaemia, oedema, and hyperlipidaemia. In contrast, Nephritic syndrome is caused by IgA Nephropathy, Post-Streptococcal Glomerulonephritis, Rapidly Progressive Glomerulonephritis (RPGN), Goodpasture’s Syndrome (Anti-GBM disease), and ANCA-associated vasculitis (such as GPA and MPA) = microvascular glomerulonephritis all presenting with haematuria, hypertension, red blood cell casts in urine, and some degree of impaired kidney function.

Answer 248

Prothrombin Time (PT): Measures the extrinsic and common coagulation pathways. Key factors: Factor I (fibrinogen), II (prothrombin), V, VII, and X. (1,2,5,7,10) Used to assess: Warfarin therapy (because it inhibits factor VII). Liver function (since liver synthesizes clotting factors). Vitamin K deficiency. Disseminated intravascular coagulation (DIC). Test result: PT is often reported as INR (International Normalized Ratio) for better standardization. Prolonged PT = deficiency or inhibition of extrinsic pathway factors (especially Factor VII), or liver disease. Activated Partial Thromboplastin Time (APTT): Measures the intrinsic and common coagulation pathways. Key factors: Factor I, II, V, VIII, IX, X, XI, XII. (1,2,5,8-12) Used to assess: Heparin therapy (which inhibits Factor Xa and thrombin). Hemophilia A (Factor VIII deficiency) and Hemophilia B (Factor IX deficiency). Lupus anticoagulant. Vitamin K deficiency (affects both intrinsic and extrinsic pathways, so both PT and APTT can be prolonged). Test result: A prolonged APTT suggests intrinsic pathway dysfunction or presence of an inhibitor. Prolonged APTT = deficiency or inhibition in intrinsic pathway factors, or heparin use.

Answer 249

If the PT prolongation is due to a factor deficiency (e.g., vitamin K deficiency, liver disease), adding normal plasma will restore the missing clotting factors. The PT will correct because the normal plasma provides the necessary factors for clotting. If the PT does not correct, it suggests the presence of an inhibitor, such as lupus anticoagulant, factor inhibitors, or anticoagulants (e.g., warfarin or heparin), that are interfering with coagulation. The inhibitor prevents the correction of PT even after normal plasma is added. e.g. aquired deficiencies

Answer 250

factor 7 deficiency

Answer 251

6 months isionaizid or 3 months comibnation rifamcin + isonizaid

Answer 252

Charcoal haemoperfusion Particularly useful in cases where toxins are highly protein-bound or not easily removed by regular hemodialysis, such as: Theophylline poisoning Phenytoin toxicity Paraquat poisoning Lithium overdose The patient’s blood is passed through a device that contains activated charcoal. The toxins in the blood are adsorbed by the charcoal as the blood flows through, effectively removing them from circulation. The treated blood is then returned to the patient’s body.

Answer 253

angiography and arterial embolization

Answer 254

because cmax quickly reached due to rapid administration sfx ototoxicity, cardiotoxicity (TDP/QTc prolongation) replaced by oral clarithromycin Erythromycin reaches a much higher peak in plasma compared to azithro/clarithro — and this high Cmax is partly responsible for dose-related toxicities, including cardiotoxicity and ototoxicity. Azithromycin achieves low plasma levels but concentrates well in tissues and phagocytes, allowing effective intracellular action with lower systemic exposure. Cmax is the highest concentration that a drug reaches in the blood plasma after dosing, before it starts to be eliminated.

Answer 255

pregablin/amitryptyline(avoid in uti and elderly)/gabapentin/duloxetine

Answer 256

OCP, vit A excess, dopamine agonists, phenytoin,abx symptoms dizziness, diplopia, headaches , Most common; often daily, diffuse, worse in the morning or with Valsalva (coughing, bending), transient visual loss, b/l papilledema Increased CSF pressure stretches pain-sensitive structures: The dura mater, large venous sinuses, and cranial nerves are pain-sensitive. Elevated pressure causes mechanical stretching and distortion, triggering pain. Worse when lying flat: Supine position causes a redistribution of CSF toward the head. This increases ICP overnight → worse headaches in the morning. Exacerbated by Valsalva (coughing, straining, bending over): These actions transiently increase ICP further, worsening the headache. Non-localised, pressure-like quality: Often described as diffuse, tight, or throbbing — not sharp or focal like in migraines.

Answer 257

iv acetazolamide + ocular massage (dislodge clot)

Answer 258

Main Infective Endocarditis Organisms Strep viridans – dental procedures Staph aureus – IVDU, nosocomial, native valves Staph epidermidis – prosthetic valves Enterococcus spp. – GI/GU procedures Strep gallolyticus (S. bovis) – colon cancer Fungi (e.g. Candida) – IVDU, immunocompromised Culture-negative – Coxiella, Bartonella, Brucella, etc. Prosthetic Valve Endocarditis Early-onset (<60 days): Staph epidermidis Staph aureus Gram-negatives Fungi Late-onset (>60 days): Same as native valve IE: Strep viridans Staph aureus Enterococcus HACEK Organisms (oropharyngeal flora) less common, slow-growing Gram-negatives) Haemophilus spp. Aggregatibacter spp. Cardiobacterium hominis Eikenella corrodens Kingella spp. Culture-Negative Endocarditis Causes Prior antibiotic use Fastidious organisms: Coxiella burnetii (Q fever) Bartonella spp. Brucella spp. Chlamydia spp. Tropheryma whipplei

Answer 259

IP gentamicin + vancomycin

Answer 260

v/q mismatch (reduced perfusion in lung tumour areas)

Answer 261

NSF is a rare, progressive fibrosing disorder that affects the skin and internal organs. It occurs almost exclusively in patients with severe renal impairment, particularly those exposed to gadolinium-based contrast agents (GBCAs) during MRI scans. Gadolinium is normally excreted by the kidneys. In renal failure, it lingers in the body — sometimes for days or weeks. That extended exposure may be enough to initiate the fibrotic cascade in predisposed individuals. Skin findings: Symmetric thickening and hardening of skin (typically lower limbs) Woody induration Hyperpigmentation Peau d’orange texture Joint contractures over time Systemic involvement: May involve: Skeletal muscles Lungs (fibrosis) Diaphragm Myocardium

Answer 262

Treponema pallidum subspecies pertenue non-venereal Transmitted by direct skin contact (not sexually), typically in warm, humid climates Primary Stage: Papule or ulcer ("mother yaw") at site of inoculation (commonly on legs) Often painless but highly infectious 🔄 Secondary Stage (weeks to months later): Multiple skin lesions: papillomas, scaly macules, crusted ulcers Bone pain: periostitis, especially in long bones Palmoplantar hyperkeratosis Mild constitutional symptoms 🦴 Tertiary Stage (years later, rare now): Gangosa: destructive lesions of nose and palate Saber shins, bone deformities, joint destruction Disfiguring but nonfatal | Test | Purpose | | ------------------------- | ---------------------------------------------------------------------------- | | **Dark-field microscopy** | Can identify *T. pallidum* in active lesions | | **Serology** | VDRL, RPR (non-treponemal) and TPHA, FTA-ABS (treponemal) — same as syphilis | | **Clinical diagnosis** | Often based on appearance + endemic setting | | **PCR** | If available, can confirm *T. pallidum pertenue* | 📝 Note: You can’t distinguish yaws from syphilis on serology alone — need clinical + epidemiologic context. Treatment (Rx) First-line: Single dose of oral azithromycin (30 mg/kg, max 2 g) Alternative (e.g. azithromycin resistance or unavailability): Benzathine penicillin G IM (50,000 units/kg, max 2.4 million units)

Answer 263

endovascular stenting (surgery is CI)

Answer 264

woman reproductive age, idiopathic disease caused by immature muscle infiltration into the bronchiolar and alveolar walls=> destruction of airways , cyst formation and progressive decline in lung function ILD , recurrent pneumothorax, chylous effusion rx = lung transplant

Answer 265

cafe au lait spots axillary/inguinal freckles 2 typical or one plexiform neurofibroma optic nerve glioma iris hamartoma (lisch nodule) sphenoid dysplasia

Answer 266

osmotically active ethanol --> hyponatremia

Answer 267

SAMS : Slurred Speech, Altered Mental status, Muscle Twitching, Seizures

Answer 268

tall slender habitus similar to marfans - kyphoscoliosis, arachnodactyl livido retiuclaris malar flush mild learning disability (none in marfans), eye lense dislocated downwards clot formation due to platelet abnormalitity, thrombosis of cerebral artery

Answer 269

=PAH not ILD (thats more diffuse Systemic sclerosis)

Answer 270

1) Myotonic dystrophy is a chronic, progressive, inherited neuromuscular disorder characterized by myotonia (delayed muscle relaxation) and muscle weakness, along with a range of multisystemic features. 2) There are two main types: Type 1 (DM1 – Steinert disease): CTG trinucleotide repeat expansion in the DMPK gene (chromosome 19). 3) Clinical features: Distal muscle weakness (hands, forearms, feet). Myotonia (especially grip and percussion). Frontal balding, ptosis, temporal wasting. Cataracts (often Christmas tree type). Cardiac conduction defects (risk of sudden death). Endocrinopathies (e.g., diabetes, hypogonadism). Cognitive impairment, excessive daytime sleepiness. Gastrointestinal dysmotility, constipation. 2) Type 2 (DM2 – Proximal myotonic myopathy): CCTG repeat expansion in the CNBP gene (chromosome 3). Onset: Usually adult. Anticipation: Less prominent than in DM1. 3) Clinical features: Proximal muscle weakness (e.g., hips, shoulders). Milder myotonia. Cataracts and cardiac issues can still occur. Generally milder than DM1. 4) Diagnosis: Genetic testing is definitive. EMG shows myotonic discharges. 5) Management: Symptomatic only – no cure. Myotonia: mexiletine or other sodium channel blockers. Cardiac monitoring (e.g., ECG, Holter). Physiotherapy and occupational therapy. Multidisciplinary care: neurology, cardiology, respiratory, endocrine.

Answer 271

stop offending cause antihistamines (chlorphenamine)

Answer 272

stop anti hypertensives for 3 weeks to get accurate measurement

Answer 273

cytotoxic t cells and then followed by fas ligand binding to fas (death receptors on keratinocytes)-> apoptosis A ligand is any molecule that binds specifically to a receptor to trigger a biological response.

Answer 274

**Acute** -- Localised rash at entry site, dry cough, wheezing, fever, eosinophilia **Chronic** - Often asymptomatic or with intermittent GI symptoms (abdominal pain, diarrhoea), eosinophilia | **Hyperinfection Syndrome** | Occurs in **immunosuppressed** (esp. steroids, transplant, HTLV-1, HIV) — massive autoinfection → sepsis, meningitis, pneumonia, multiorgan failure Ivermectin is first-line (usually 2 days, longer for chronic/hyperinfection) or alvendazole

Answer 275

After insulin initiation, glucotoxicity and lipotoxicity decrease, relieving stress on surviving beta cells These cells temporarily recover some insulin production The immune destruction continues in the background, so it’s not a cure — just a pause in disease progression Occurs weeks to months after initiating insulin therapy in T1DM Characterized by improved glycaemic control with minimal insulin Can last a few weeks to up to 1–2 years, though most commonly lasts a few months continue basal insulin and change other insulin

Answer 276

CTLA-4 immune checkpoint inhibitor (blocks t - cell inhibitory signals => increased number of reactive t-effector cells which mount t-cell immune response to tumour cells)

Answer 277

e.g hashimotis not thyroxine replacement until r/o autoimmune adrenal insufficiency (send 08:00 cortisol), as if you give In undiagnosed Addison’s disease, the body lacks sufficient cortisol. Thyroxine increases metabolic rate, which: Increases cortisol clearance Increases tissue demand for cortisol If the adrenal glands can't meet this demand, the patient can rapidly decompensate into an adrenal crisis: Hypotension, hypoglycaemia, shock, coma, and even death pulsed oral betnametasone (3-6 months) + NBUVB (2x/week) for vitiligo vitiligo, hypothyroid sx anti thyroglobulin, antimicrosomial

Answer 278

nsaid, colchicine, pred, dapsone

Answer 279

Paroxysmal Hemicrania Definition: A type of trigeminal autonomic cephalalgia (TAC) characterized by frequent, short-lasting, strictly unilateral headaches with autonomic features. Clinical Features: Severe, strictly unilateral pain (typically orbital, supraorbital, or temporal) Duration: 2 to 30 minutes Frequency: typically more than 5 attacks per day Associated ipsilateral autonomic symptoms: lacrimation, conjunctival injection, nasal congestion, ptosis, miosis, facial sweating More common in females Diagnostic Feature: Complete response to indomethacin (diagnostic criterion) Diagnosis: Clinical diagnosis Confirmed by therapeutic trial of indomethacin (usually 25–75 mg/day) Brain MRI may be used to exclude secondary causes Treatment: First-line: indomethacin, starting at low dose and titrating up (e.g., 25 mg TID) Consider proton pump inhibitor (e.g., omeprazole) for gastric protection

Answer 280

tenofovir (NRTI) interferon CI in decompensated LD

Answer 281

in late pregnancy - because of recommended risk of hepatotoxicity ( can use carbimazole)

Answer 282

Type 1 - Primary adrenal insufficiency (Addison's disease) - Hypoparathyroidism - Chronic mucocutaneous candidiasis (often first sign) Type 2 - Primary adrenal insufficiency - Autoimmune thyroid disease (Hashimoto’s or Graves’) - Type 1 diabetes mellitus

Answer 283

1. native valve = amoxicillin and gent 2. pros valve = vanc, rifampcin, gent 3. SA = fluclox 4. strep = ben penc 5. hacek = cephalosporin

Answer 284

toxic shock syndrome.. TSS is a life-threatening, toxin-mediated illness most commonly caused by Staphylococcus aureus or Streptococcus pyogenes (Group A Strep). Prompt recognition and aggressive treatment are essential. IVF, vaso pressors, source control - e.g. tampon, surgical debridement, abx, IVIG to neutralize superantigen

Answer 285

indium labelled white cell scan

Answer 286

calcium deposits in cutaneous arteries leading to thrombosis and ischemic necrosis, refractory ulcers in abdo, lower legs, buttocks

Answer 287

if vaccinated: today and day 3 if not: today, day 3 , 7, 14 , 30 + RIG

Answer 288

schamberg disease - due to exercise/chronic venous insufficiency/ long distance running - progressive pigmented purpura

Answer 289

bisoprolol

Answer 290

plasmapheresis if symptomatic

Answer 291

3,4 diaminopyridine fIn LEMS, antibodies attack presynaptic voltage-gated calcium channels (VGCCs) → reduced acetylcholine (ACh) release at the neuromuscular junction. 3,4-DAP blocks voltage-gated potassium channels → prolongs depolarization of the nerve terminal → enhances calcium influx → increases ACh release.

Answer 292

Cutaneous Mastocytosis Most common form in children. Presents as urticaria pigmentosa: small brown macules or papules that urticate (become red and swollen) when rubbed → Darier’s sign Usually self-limiting 🧓 Systemic Mastocytosis (SM) Involves bone marrow and other organs. Associated with KIT D816V mutation (diagnostic marker) May be indolent, smouldering, or aggressive Mast cells are immune cells derived from the bone marrow. They contain histamine, tryptase, prostaglandins, and other chemical mediators involved in allergic reactions, inflammation, and anaphylaxis. Symptoms of Mastocytosis: Skin: flushing, itching, urticaria pigmentosa, Darier’s sign Gastrointestinal: nausea, vomiting, abdominal pain, diarrhea Cardiovascular: hypotension, syncope, anaphylaxis Skeletal: bone pain, osteopenia, fractures Bone marrow involvement: anemia, leukopenia, thrombocytopenia in aggressive forms Investigations: Serum tryptase (usually elevated >20 ng/mL in systemic cases) Skin or bone marrow biopsy to demonstrate mast cell infiltration Genetic testing for KIT D816V mutation Treatment: H1 and H2 antihistamines for flushing, pruritus, GI symptoms Mast cell stabilizers such as sodium cromoglicate Omalizumab (anti-IgE) in cases with frequent anaphylaxis Midostaurin (a tyrosine kinase inhibitor) for aggressive systemic disease Epinephrine auto-injector for patients at risk of anaphylaxis

Answer 293

Alteplase is a recombinant tissue plasminogen activator (rt-PA) Binds to fibrin in a thrombus (clot) Converts plasminogen → plasmin Plasmin breaks down fibrin → fibrinolysis (clot breakdown) Fibrin-specific: Preferentially activates plasminogen bound to fibrin (less systemic bleeding vs older agents like streptokinase - causes hypotension too) Rapid clot dissolution: Restores perfusion in occluded vessels so summary: Alteplase → activates fibrin-bound plasminogen → forms plasmin → digests fibrin → dissolves clot

Answer 294

Zieve’s syndrome is a rare, under-recognized condition characterized by a triad of: Hemolytic anemia Jaundice Hyperlipidemia It typically occurs in the context of heavy alcohol use, particularly during alcoholic hepatitis or acute alcohol withdrawal.

Answer 295

fingolimod (prevents lymphocytes across BBB less dmg to oligodendrocytes)

Answer 296

parasitic flukes hepatosplenic or urogenital (bladder haematuria) or acute katayama fever

Answer 297

🧪 Adrenaline in Cardiac Arrest Mechanism: Alpha-1 agonist → vasoconstriction → ↑ coronary & cerebral perfusion. Beta-1 agonist → ↑ heart rate, contractility, and automaticity. Amiodarone in Cardiac Arrest Mechanism: Class III antiarrhythmic → blocks K⁺ channels → prolongs repolarization. Also has Na⁺ channel blockade, weak beta-blockade.

Answer 298

causes renal artery stenosis and flash pulmonary edema in young ptx (non atherosclerotic, non-inflammatory disease causing renal artery stenosis) In patients with bilateral renal artery stenosis due to fibromuscular dysplasia, flash pulmonary edema can occur because of: ↓ Renal perfusion → activation of RAAS ↑ Angiotensin II → severe hypertension ↑ Afterload + fluid retention → acute LV failure ↑ LV end-diastolic pressure → ↑ pulmonary capillary pressure → Fluid leaks into alveoli → flash pulmonary edema

Answer 299

GuHCl can denature botulinum toxin (Guanidine Hydrochloride ) + trivalent antiserum (against 3 strains of c. botulinism)

Answer 300

Mnemonic: "ALP RISES" A — Adolescents / Aging / ALP isoenzymes Normal in growth spurts (children, teens) Placental ALP in pregnancy Healing fractures L — Liver (cholestasis) Biliary obstruction (stones, stricture, tumour) Primary biliary cholangitis (PBC) Primary sclerosing cholangitis (PSC) Drug-induced liver injury P — Paget’s disease Disorganized bone remodelling Often very high ALP R — Rickets / Osteomalacia Vitamin D deficiency Soft, poorly mineralized bones I — Infiltrative liver disease Tumours (HCC, metastases) Sarcoidosis, amyloidosis, TB S — Secondaries (bone mets) Prostate, breast, lung cancer metastasising to bone E — Endocrine (e.g. hyperparathyroidism) Increased bone turnover S — Surgery / Sepsis / Stress Post-op healing Sepsis with hepatic dysfunction

MRCP Part 2 Flashcards

MRCP Part 2 Revision (334 cards)