Clinical Flashcards

1
Q

John Conner a recent patient of yours has a lot of stress from his daily life which hasn’t improved over the course of time he’s been meeting with you. You decide to start him on anti-hypertensive medication. You know from his history that he has chronic kidney disease. What should you prescribe him? A) ACEI B) Thiazide C) CCB D) yoga

A

A is correct Chronic kidney disease- start on angiotensin converting enzyme inhibitor (ACEI) or angiotensin receptor blocker (ARB) African American- start with Thiazide-type diuretic or calcium channel blocker (CCB) Everyone else can start with either: ACEI, ARB, or CCB

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2
Q

Doing routine physical exam of one of your adolescent patients who’s been complaining of leg pain during exercise at school you notice they have cold legs and what sounds like a heart murmur. You decide to check their bp in both their arm and leg and notice a 25mmHg difference in pressure, with the legs having the lower bp. How should you diagnose this condition? A) CT B) Ultrasound C) MRI D) Transthoracic echo

A

D) is correct They likely have coarctation of the aorta

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3
Q

You’re looking at some cross sectional anatomy laying on the desk of your physician friend and see a large mass on the top of the kidney. He says the patient has been having aniexty and headaches lately. Which hormone is likely causing these problems? What tests would you order? A) Tyrosine B) Epi C) NE D) ADH E) Aldosterone

A

C) NE This is likely pheochromocytoma which is an adrenal glad tumor secreting hormones; predominately NE (though Epi is a good second guess) Classic triad of symptoms: Headache, perspiration, and palpitations Test: 24 urine sample and plasma looking at hormone levels

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4
Q

You go to the lab to flirt with the on call nurse and notice a lab report for renin and aldosterone levels. Looking at the ratio of these two molecules is a diagnostic test for which condition? A) Hirsutism B) Pheochromocytoma C) Chrons D) Cushings E) Primary aldosteronism

A

E) primary aldosteronism Signs/symptoms are - hypokalemia, hypernatrimia and resistant hypertension

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5
Q

You have a hypertensive patients records indicate they had a diagnostic test called a polysomnography. What hypertensive issue may have been under investigation? A) Cushings B) polylipidemia C) Pheochromocytoma D) Coarctation of the aorta E) OSA

A

E) OSA obstructive sleep apnea Signs-snore, daytime sleepyness, apneic events at night Other tests-sleep score (Epworth sleepiness scale), pulse oxygen

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6
Q

Your first pediatric patient presents with leg swelling and has high bp. What follow up questions should you ask? With this information alone what test might you order to cover your basis since 85% of pediatric patients with hypertension have a disease with similar symptoms?

A

Do you have very foamy urine Test: BUN, Urinalysis, urine culture, renal ultrasound (likely small kidney on one side) They likey have renal parenchymal disease

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7
Q

According to the JNC 8 guidlines for hypertension at whay bp should you start someone on medication who is 43 y/o ? What if they’re 83 y/o?

A

>140/90 >150/90 > or equal to

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8
Q

What are the major risk factors for coronary heart disease CHD?

A

CHLOE cigarettes Hypertension Low HDL Old age Elder/family history

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9
Q

How do you insure an accurate bp? What are the steps?

A

Patient wait 5 mins with feet on ground proper size cuff 2/3 arm encircled Inflate about 20mmHg above systolic value avoid caffeine smoking etc beforehand Take 2 per visit (or at home, walgreens to avoid white coat htn) Take 2-3 x week for accurate numbers

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10
Q

Define the parameters of both hypertensive crisis and hypertensive urgency?

A

Hypertensive crisis is diastolic bp >120 plus end organ damage (indicate secondary htn) Hypertensive urgency there are no signs of end organ damage

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11
Q

What percentage of hypertension is primary vs secondary and what are the characteristics of each?

A

primary 95% Onset 20-50 y/o family history of htn no features of secondary htn no end organ damage secondary 5% 20 y/o or younger and 50 y/o or older No family history Acute severe end organ damage indicated with labs

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12
Q

Nearly all genes identified with the pathogenesis of primary hypertension involve what? A) congenital heart defects B) Atherosclerosis C) beta blocker use D) Impaired kidney sodium excretion D) baseline rates of albumen are high

A

D) impaired Na+ excretion in the kidney

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13
Q

What is your main focus when trying to diagnose someone with hypertension?

A

To determine if they have any signs of secondary htn. Lots of investigation into whether they have any end stage organ damage.

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14
Q

What are the 4 cardinal findings of shock? Explain each

A
  1. Hypotension systolic less than 90mmHg 2. oliguria (low urine output) blood shunting from kidneys 3. metal status change- aggitated to coma 4. metabolic acidosis- decrease in lactate being cleared due to liver and kidney failure (lack of O2, decreased perfusion).
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15
Q

How to you treat a patient with shock?

A
  1. VIP ventilation- O2 usually intubation Infuse- fluid resuscitation pump- vasoactive drugs (make sure the pump is full before you try to squeeze the vessels) 2. diagnose and treat at the same time 3. Arterial catheter if needed (blood gas) 4. Central venous catheter for fluid, drugs, measure CVP
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16
Q

What are some examples of obstructive shock?

A

pulmonary hypertension pulmonary embolism cardiac tamponade-fluid in pericardial sac tension pneumothorax constrictive pericarditis

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17
Q

You have a patient admitted that is sweating and feverish. Their blood pressure is 85/43 and they look ill. You see what looks to be an infected cut on their right leg. What lab tests would initially NOT be indicated? A) ABG B) BUN C) Blood culture D) CBC w/differential E) Potassium

A

E- all the others are appropriate when suspicious of septic shock. BUN is checking for kidney function ABG is arterial blood gas

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18
Q

You have a patient come into the clinic complaining of chest pain and your attending asks you which life threatening etiologies you need to r/o. What’s your response?

A

Heart: MI, aortic dissection, aortic stenosis Lungs: Pneumothorax, pulmonary embolism GI: perforating ulcer, esophageal rupture

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19
Q

Your patient comes to you complaining of fatigue, stating that “ I just get out of breath more easily when I’m going up stairs.” Upon auscultation of the chest you hear a holosytolic murmur and EKG shows a slight L axial deviation. What is a primary cause of this valvular disease? A. Ischemia B. Hypertrophic cardiomyopathy C. Infective endocarditis D. marfans syndrome

A

C. infective endocarditis. The valvular disease is mitral regurgitation. A and B are secondary causes D is associated with aortic dissection and other elastic tissue problems.

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20
Q

High pitched diastolic murmur (blowing) with water hammer pulse. heard best at erbs pt.

A

Aortic insuffiency/regurg

21
Q

How would you detect mitral stenosis on auscultation and EKG?

A

Low-pitched diastolic rumble murmur Enlarged P wave indicated LAH Chest pain secondary to pulmonary htn, decreased exercise tolerance Common association: Rheumatic heart disease

22
Q

What’s the most common valvular disease of the elderly?

A

Aortic stenosis

23
Q

O2 decrease in the heart due to an ischemic event can lead to angina. What’s the typical duration of that pain? 1 min 3-5 min 10 min 22min

A

3-5 min 1 min or less unlikely cardiac more than 20 mins usually leads to an MI

24
Q

How is angina usually described?

A

squeezing burning tightness choking. Not always pain 60% of these patients will have normal EKGs

25
A person with stable angina is usually assessed for their risk of developing CAD by doing what? When should you treat with drugs?
EKG to check for valvular disease, THEN a stress test to asses for ischemia. Eval LV function. If there is ischemia, LV dysfunction may need coronary angiography to take a look.
26
What is meant by acute coronary syndrome?
continuum of myocardial ischemia Unstable angina NSTEMI STEMI If this is the diagnosis: ACT FAST. You have more time for the USA, and NSTEMI, compared to the STEMI
27
Describe the 3 different causes of ACS
Unstable angina- EKG changes indicate some ischemia, no elevation in cardiac biomarkers. NSTEMI- Same as unstable angina except there is an elevation in cardiac biomarkers STEMI- Direct evidence of MI on EKG. ST elevation, cardiac biomarker elevation.
28
Which cardiac biomarkers are best for determining a MI?
Troponin is best, followed by CK-MB (specific for muscle; including skeletal), then myoglobin (non-specific tissue breakdown)
29
When should you draw labs for cardiac biomarkers and why?
When the patient presents and then 6-9 hrs later. Early measurement maybe below threshold sensitivity until the 6 hr mark. Usually tissue takes 1-3 hrs to necrose.
30
How do you treat unstable angina or a NSTEMI?
anti-platlet/anti coagulant therapy, catheterization to place a stent or use balloon angioplasty.
31
How do you treat a STEMI?
Reperfuse! Cardiac angiography within 90 mins Treat with Fibrinolysis
32
The dominant branch of the coronary arteries is determined how? Why do we care?
The posterior interventricular branch which can be associated with the R or L coronary artery. We care b/c depending on its location an infarct upstream which occludes this artery, along with ether the R or L coronary artery, will cause more ischemic damage. A widow marker is an upstream occlusion that affects two major coronary branches.
33
What's the big deal with "end" arteries?
End arteries have no anastamosis to help provide collateral blood supply should the artery become occluded. This is dangerous for the tissue at the end of the line. End arteries are in the heart (coronary arteries), kidneys. and retina among other places.
34
What is the most common cause of secondary htn? Name some additional causes.
Kidney disease Vascular disorders: Arteriosclerosis Pheochromocytoma- adrenal gland tumor ETOH 3+ daily Meds- contraceptives, decongestants Brain lesions- increase incracranial pressure and trigger increased systemic bp so blood can perfuse the brain tissue.
35
What histological changes do you see with the heart with systemic hypertension?
Heart needs to get larger to push blood against the high systemic pressure. These new myocytes need oxygen but many end up dying from ischemia and being replaced by fibrous tissue that doesn't contract properly. Characteristic box shaped nuclei
36
How does atherosclerosis occur?
Tunica intima is irritated (smoking, hyperlipidemia, or high bp) The tunica intima is damaged allowing LDL to breach this endothelial layer and squeeze between it and the tunica media. Macrophages get activated and goarge themselves on LDL until they die (foamy Macrophages)= lake of fat/fatty streak. Smooth muscle migrates into the intima and make a fibrous cap (scab over the streak) which decreases vascular compliance Smooth muscle cells lay down Ca2+
37
What are the gross features of malignant htn and the most common demographic to have it?
**Gross features** encephalopathy, renal disorders, vascular changes, papilledema. _Kidney_: size varies, red areas of hemorrhage and hyperplasia of arterioles (onion skin arteriolitis), fibrinoid necrosis of arteriole. **Demographics** Disease of middle aged adults (40 y/o) m more than f. esp. young black men, persons with chronic renal disease and toxemia of pregnancy.
38
Where are the most common sites of intercerebral hemorrhage, caused by htn encephalopathy?
Basal Ganglia-thalamus 75% Pons 15% Cerebellum 10%
39
Describe hypersensitive encephalopathy and how it lead to lacunar infarts. What are these such a problem?
This condition is the result of maligant htn which can be brought about by various causes: eclampsia, renal nephritis ... One theory is that the autoregulation of the brain is unable to compensate for this drastic increase in bp and vasospasm occurs causing occlusion and ischemia. (Blood vessels in the brain normaly respond to high blood pressure through constriction). This ischemia can cause thromboses of small arterioles with fibrinoid necrosis or lucunar infarts. Problems range from forgetfullness, dementia, or coma
40
What's the most severe concequence of hypertensive encephalopathy?
Charcot bouchard aneurysm Intercerebral Hemorrhage caused by the rupture of small aneurysms.
41
What is AV nicking? Whose at risk and how does it progress?
Arteriovenous nicking occurs in the retina due to hypertension and appears where athrosclerotic arterioles cross veins that appear kinked. This appearance is described initally as a copper wire b/c of the think plaque that narrows the lumen and reflects light differently than a normal arteriole. If it progresses it will look like parallel lines or silver wire.
42
How does one get CHF? What symptoms might you notice?
Chronic progressive ischemia=decreased perfusion of the heart=CHF The ischemia is due to atherosclerotic plaque formation Ischemia may present with angina-stable or unstable
43
Identify the which artery is occluded based on the location of the infarct, and where you would see this on EKG Anterior wall Lateral wall Posterior wall inferior wall
Anterior=LAD EKG- Q waves and ST eleveation in leads V1-V4 Lateral=Circumflex EKG-Q waves in leads I and AVL Posterior=RAD EKG- ST depression in V1-3 Inferior=R or L terminal branch depending on which is dominant EKG- Q waves in II, III, and AVF
44
Transmural infarcts are caused by \_\_\_\_\_80-90% of the time What percentage of people die from this? What happens to the rest?
Thrombsosis of a coronary artery (other causes: embolized plaque, vasospasm) 25% mortality 75% survive and most develop Heart failure of cardiogenic shock Worry about brain and kidneys post MI. kidney most common, brain most dangerous
45
Name and describe the 2 types of MI
Transmural- all 3 heart layers. may involve IV septum subdendocardial- infarct is concentric around the subendocardial layer
46
What are the microscopic and macroscopic finding for acute MI?
MICRO Cell death Acute inflamamtion and PMNs neutraphils (acute) Granulation tissue (angiogenesis) and macrophages (eat necrotic debris) (subacute) Necrotic myocardium replaced with fibrous scarring (chronic) MACRO 1-2 days infarct becomes yellow with a hemorrhagic rim (acute) 1-2 wks granulation tissue (blood vessels) makes area pink (subacute) Thereafter white fibrosis predominates (chronic)
47
What are some classic changes on EKG related to an acute MI? What are some classic metabolic changes?
Long Q waves, elevated ST segment, and inverted T waves Metabolic changes include-lactic acid production leading to acidosis Necrotic cell membranes leak K+ and cause hyperkalemia
48
What are the 3 major complications of MI, describe each?
_Worst complication is **Myocardial Rupture**_: This occurs when blood in the ventrible under high pressure penitrates through the necrotic myocardium and into the pericardial sac which can compress the heart. This is called cardiac tamponade and can lead to cardiac standstill; typically occurs about 1 wk post MI. **LV aneurysm:** Fibrous tissue that replaces dead myocytes cause irregular contraction of the heart and can form a ventricular aneurysm. **Mural thrombus (wall clot):** Endocardium is often damaged by MI and blood coagulates with the necrotic endocardium forming a thrombus. This may weaken contaction and impede blood flow leading to CHF. Embolization is another concern.
49
What is a LIMA bypass and a CABG bypass surgery?
LIMA is the left internal thoracic (formerly mammary) artery connecting to the LAD artery (usually) CABG coronary artery bypass graft connects aorta, subclavian or both to Right or left coronary arteries