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Ventricular Septal Defect

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Atrial Septal Defect

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Patent Ductus Arteriosus

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Gallstone Ileus

stone erodes through the gallbladder in to the duodenum

formation of fistula leads to air in biliary tree (pneumobilia)

stone obstructs bowel, usually in terminal ileum

Right iliac fossa calcification (gallstone) possibly lodged at the ileocaecal valve

Pneumobilia - see RUQ

Dilated loop of small bowel indicating small bowel obstruction

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TIMELINE: MI Complications

0-24h: 

Ventricular arrythmias

RV failure

HF

Cardiogenic shock

1-3d:

Post MI fibrinous pericarditis

1-5d: 

Papillary muscle rupture --> severe Mitral regurgitation

IV septum rupture (L->R shunt)

5d-2w: 

Free wall rupture (tamponade)

2w-Several months:

LV aneurysm

Dressler Sd

Myocardial infarction

3 cardinal signs:

Elevation of ST segment

Inversion of T wave

Deep & wide Q wave

With reciprocal changes in the leads facing the opposite wall:

Depression of ST segment

Tall, upright T waves

Changes do not appear at the same time. It happens in this order:

Elevation of ST segment stays for 2-3d and gradually goes back to base level in 1-2w

T wave becomes inverted after 2 days, and remains like that for 3w, and gradually becomes flat and then upright over 2-3m

Q wave = muscle death, appears after 1 week, and gradually deepens and remains permanent. Size proportional to size of infarct.

Timeline:

1°d: ST segment elevation + tall T wave

2-3°d: ST segment still elevated + T wave slowly becomes inverted

7°d: ST segment starts returning to base level + T wave inverted + Q wave starts appearing, it deepens. (If ST segment stays elevated >6m, think of development ventricular aneurism)

3°w: Q wave fully developed + T wave starts becoming flat

End of 3m: only Q wave stays the same, ST segm and T wave return to normal. If the size of the infarct was small, Q wave goes back to normal.

Coronary Arteries, branches & supply:

Localization of infarct:

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Coronary Arteries in a nutshell

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Do not let someone else’s success get in the way of your progress. Always celebrate other people ’s success as well as continuing to work on your own craft. Please don’t determine your self worth by the amount of time it takes to you to get to where you want to be and who you want to be. Enjoy this journey and keep working hard.

:)

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CHEMO MAN 2.0

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Poeta uruguayo, Mauricio Saravia. Photo from www.lukeford.net posted on Wikimedia Commons in 2008. Another notabe case in a teenager from Haiti.

The three words of McCune-Albright disease:

The most famous (mouthfull) words of the condition: Polyostotic Fibrous Dysplasia. What that means is that the bone will grow tumor-like fibrous (scar) tissue instead of the normal medullary (bone marrow) bone tissue. Irregular Bony trabeculae That will cause the deformities that make the disease famous. It’s caused by mutation in the gene GNAS1 and affects mostly the extremities. Not cancerous. Mosaic G protein signaling mutation 

Premature puberty in girls. It can affect boys as well, but the question stem in exams tend to report female cases, like a 2-year-old with menstrual bleeding. Early puberty is one of the many endocrine problems of these patients and a favorite to put in exams. Other problems include over-reactivity of the thyroid, pituitary and adrenal glands (hyperthyroidism, acromegally and hypercortisolism). 

And, of course, Café-au-lait spots. The interesting feature is the tendency for the lesions to not cross the body’s midline.

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MCC of an isolated, asymptomatic elevation of ALKALINE PHOSPHATASE in an elderly patient.

Laboratory markers for bone turnover are elevated: PINP (procollagen type I N-propeptide or just remeber that song from 50cent “pimp”), urine hydroxyproline

Imaging: XR (osteolytic or mixed lytic/sclerotic lesions), radionuclide bone scan (focal increase in uptake, also for staging)

Tx: bibphosphonates

Paget Disease or Osteitis Deformans

Disorder in bone remodeling, 3 stages

Osteolytic (osteoclasts)

Mixed (osteclasts & osteoblasts)

Osteosclerotic (osteoblasts, “burn-out”)

Mosaic pattern on lamellar bone, big skull (no hat fits), foraminal narrowing (cranial nerve impingement), bone fractures, bone pain, warmth (increase vascularization).

Complications: AVshunt within bone marrow, can cause high output, cardiac failure, osteosarcoma

Possible underlying mechanism: Paramyxovirus infection of osteoclasts

Lab: Normal Calcium and Phosphate, INCREASED ALKALINE PHOSPHATASE

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Diuretics: Site of action & Mechanism

Osmotic Diuretics: =/=> water reabsorption throughout the tubules, but mostly in the proximal tubule (mannitol)

Carbonic Anhydrase Inhibitors: proximal tubule, =/=> C.A (acetazolamide, dorzolamide)

Loop Diuretics: thick ascending loop of Henle, =/=> Na+/K+/2Cl- transporter (furosemide, ethacrynic acid)

Thiazides: early distal tubule, =/=> Na+/Cl- symporter (hydrochlorothiazide, indapamide)

K+ sparing agents: distal nephron (late distal tubule + colecting ducts). Aldosterone receptor antagonist (spironolactone) or =/=> Na+/K+ exchange by =/=> of Na+ channels (amiloride, triamterene)

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I can be changed by what happens to me, but I refuse to be reduced by it.

Maya Angelou (via wordsnquotes)

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To cure sometimes, to relieve often, to comfort always.

Edward Livingston Trudeau (via themedicalchronicles)

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Newborn Respiratory Distress