Advanced Editing (pics/ sounds) Flashcards
(Heart embryo) What does the truncus arteriosis become?
Truncus Arteriosis—> The ascending aorta and the pulmonary trunk
(Heart embryo) What does the bulbous cordis become?
Bulbous cordis—> The smooth outflow tracts of the RV and LV (example: forms the infundibulum/ conus arteriosus= smooth muscle funnel from RV to pulmonic arteries)
(Heart embryo) What does the primitive ventricle become?
Primitive Ventricle—> The trabeculated part of the RV and LV
(Heart embryo) What does the primitive atrium become?
Primitive Atrium—> The trabeculated part of the RA and LA
(Heart embryo) What does the right horn of the sinus venosus become? Left horn of the sinus venosus?
Right horn—> smooth part of the RA (sinus venarum)
Left horn—> Coronary sinus
(Heart embryo) What do the endocardial cushions become?
They contribute to the formation of the atrial and ventricular septum and all the valves (**defects of this are common in Down syndrome)
What does dextrocardia mean?
Your heart is on the right side of your chest
What is this?
Aortic regurgitation (aortic pressure is falls in diastole- when blood is leaking back from the aorta to the LV)
What is this?
Aortic stenosis (LV pressure has to get really high compared to aortic pressure to push blood through the stenotic aortic valve)
What is this?
Mitral regurgitation (LA pressure is only high during systole when blood from the LV flows back into the LA as it’s trying to pump)
What is this?
Mitral stenosis (LA pressure is always higher to get blood through stenosed valve to the LV)
What kind of cells in embryo are involved in forming the atriopulmonary septum (to separate the pulmonary arteries and aorta)?
NCC’s (neural crest cells) & endocardial cells (**truncal abnormalities like transposition of the great vessels, tetrology of Fallot, and persistent truncus arteriosis are due to NCC’s not being able to migrate)
What’s the difference between eccentric and concentric hypertrophy?
Describe the mechanism of Digoxin (digitalis).
Digoxin inhibits the K+/Na+ pump on myocytes—> increases Na+ in the myocytes—> makes the Na+/Ca2+ pump not work as well because Na+ won’t want to come into a high [Na+] environment—> build up of Ca2+ in the myocyte available for contraction= increases contractility
EKG: what is the P wave? QRS? T wave?
P wave= atrial depolarization
QRS= ventricle depolarization (atrial repolarization embeddded in here)
T wave= ventricle repolarization
EKG: what does the PR interval tell you?
PR interval= AV conduction delay (the AV node slows the rate of conduction and this shows it because it is the interval where atrial depolarization is spreading to the AV node—> ventricles for contraction)
EKG: What does the QRS interval tell you? How about the QT interval?
QRS interval= speed of ventricular excitation (if wide that means the ventricles are depolarizing slowly—> slow HR)
QT interval= period of ventricular excitation and refractoriness (the entire systole= depolarization + depolarization)
EKG: what does the ST segment mean? What does R to R mean?
ST segment= plateau phase where ventricles are fully depolarizer and refractory (before ventricular repolarization)
R to R segment= ventricular diastole (ventricles are relaxing and refilling with blood **note: R to R segment includes the T wave which is ventricle repolarization and repolarization is technically part of contraction, but it’s starting to relax at this point)
What is the conduction pathway (order of the spread of excitation through the heart)?
SA node—> atria—> AV node—> bundle of His—> right and left bundle branches—> Purkinje fibers—> ventricles (apex and then rest of ventricles)
When might you see a U wave following a T wave on EKG?
U waves- in hypOkalemia or bradycardia (slow HR)
What might a T wave inversion on EKG indicate?
Ischemia or recent MI (T wave= ventricular repolarization)
What’s a normal PR interval? What’s a normal QRS interval?
Normal PR interval= 3-5 small boxes (<200 msec)
Normal QRS interval= <3 small boxes (<120 msec)
Describe how the myocyte action potential graph (showing electrical activity of a single myocyte) matches up with an EKG reading (showing electrical activity across lots of myocytes).
Phase 4 (ventricular diastole) matches up with the P wave (atrial systole= ventricular diastole). Phase 0 (ventricle depolarization) matches up with QRS (ventricle depolarization). Phase 2 (refractory period) matches up with the ST segment (ventricles are fully depolarizer & refractory). Phase 3 (ventricle repolarization) matches up with the T wave (ventricle repolarization). REMEMBER THIS: the EKG from Q- T (QRS and T wave= ventricular repolarization and depolarization) matches up to phase 0-3 (ventricular systole) and the P wave and flat part (ventricular diastole) matches up to phase 4 (ventricular diastole).
What is the difference between ASD (atrial septal defect) and PFO (patent foramen ovale)? Which is more likely to cause a paradoxical emboli?
ASD= ostium/ foramen secundum or (more rarely) ostium/ foramen primum don’t form properly—> hole in the atrial septum between the RA and LA
PFO= ostium/ foramen secundum or ostium/ foramen primum don’t fuse (in 25% of people)—> hole in the atrial septum between the RA and LA
PFO is more likely to cause a paradoxical emboli (blood clot using shunt to move from RA—> LA, bypass lungs, and become systemic leading to a stroke)
*note that PFO is present in 25% of people- usually doesn’t cause problems, but paradoxical emboli is the one potential problem it can cause. ASD is more rare and requires surgery so the shunt doesn’t reverse directions (Eisenmenger syndrome)
Explain Rheumatic Herat disease: (1) Mechanism, (2) what heart problem you usually get + what you see on histo, and (3) what it can develop into.
(1) Mechanism: you get Rheumatic fever and 2-4 weeks later develop heart problems due to a type II hypersensitivity immune response. Strep A antibodies cross-react with cardiac myocytes (even though they should only attack the M protein, they attack the heart too bc M proteins look similar, called “molecular mimicry”). (2) Most common to get: mitral valve regurgitation. You see Aschoff bodies (granuloma with giant cells) on histo. (3) Can progress to: mitral valve stenosis (the infection damages the valve and overtime of constant regurgitation, the damage leads to hardening. Aschoff bodies are replaced by fibrous scar tissue.)
In embryo, there are 6 pharyngeal arches that are each associated with a cranial nerve, aortic arch, and musculoskeletal structure(s). What are the derivatives of the 6 aortic arches (i.e. what vessels do they each develop into)?
1st—> part of the maxillary artery
2nd—> hyoid artery and stapedial artery
3rd—> common carotid artery and proximal internal carotid artery
4th—> on left: aortic arch; on right: proximal right subclavian artery
6th—> proximal pulmonary arteries and on left: ductus arteriosus
(*note: there is no 5th aortic arch)
What murmurs are heard best at the 2nd intercostal space on the right/ right upper sternal border (aortic space)?
aortic stenosis, aortic valve sclerosis, physiologic murmurs
What murmurs are heard best at the left sternal border?
Diastolic: aortic regurgitation, pulmonic regurgitation
Systolic: hypertrophic cardiomyopathy
What murmurs are heard best at the 2nd intercostal space on the left/ left upper sternal border (pulmonic area)?
Systolic ejection murmurs: pulmonic stenosis, flow murmurs
What murmurs are heard best in the left lower sternal border (tricuspid area)?
Holosystolic murmurs: tricuspid regurgitation and VSD
Diastolic: tricuspid stenosis and ASD
What murmurs are heard best at the apex/ 5th intercostal space at the mid-clavicular line (mitral area)?
Holosystolic murmur: mitral regurgitation
Systolic: mitral valve prolapse (MVP)
Diastolic: mitral stenosis
What are the “5 terrible T’s?” Note: these are the congenital heart problems that are right—> left shunts that cause early cyanosis (“blue babies”). For all these conditions, you need to give Prostaglandins (PG’s) to keep the ductus arteriosus open until the baby can get surgery to correct the problem.
- Truncus Arteriosus (1 vessel) Truncus Arteriosus fails to divide into separate pulmonary trunk & aorta.
- Transposition (2 switched vessels) Aorta and pulmonary artery flip flopped so that the heart has 2 independent circuits.
- Tricuspid Atresia (3= Tri) Tricuspid valve fails to form.
- Tetralogy of Fallot (4= Tetra) Pulmonary infundibular stenosis, RV hypertrophy, Overriding aorta, and VSD.
- TAPVR= Total Anomalous Pulmonary Venous Return (5 letters in the name) Blood from the lungs dumps back into the right heart.
The spot where the frontal, parietal, temporal, and sphenoid bones meet in the skull is called what? It is more vulnerable to fracture. If it fractures, what is the patient at risk for?
The Pterion. Fracture can penetrate the middle meningeal artery (branch off of the maxillary artery) and cause a epidural hematoma (bleeding between dura matter and the skull).
The middle meningeal artery is a branch off of what artery?
The maxillary artery.
Short stature, short thin neck, broad chest, and shortened 4th metacarpals. What are you thinking? What congenital heart defect(s) is/ are most likely?
Turner syndrome. Most likely to have bicuspid aortic valve and/ or coarctation of the aorta.
The right pulmonary artery is _____ to the right bronchus. The left pulmonary artery is _____ to the left bronchus. (Fill in with anterior, posterior, superior, or inferior)
The right pulmonary artery is ANTERIOR to the right bronchus. The left pulmonary artery is SUPERIOR to the left bronchus.
What are the 4 causes of hypoxia?
Hypoxia= low oxygen to tissues
Causes:
1) dec cardiac output (CO)
2) hypoxemia
3) anemia
4) CO poisoning
What are the 5 causes of hypoxemia? Specify the effect they each have on the A-a gradient.
Hypoxemia= low oxygen in blood. Causes:
Normal A-a gradient (gas exchange is fine- problem is external):
1) high altitude
2) hypoventilation (includes opioid use)
High A-a gradient (air trapped in lung alveoli, not getting into capillaries):
3) V/Q mismatch
4) diffusion limitation (like fibrosis)
5) right-to-left shunt
Which flow volume loop will look like the same shape as normal but smaller? Which one will look like a dinosaur? (Options: restrictive lung dz and obstructive lung dz)
restrictive lung dz (problem getting air in)—> flow volume loop looks normal, but smaller (less air in= less air out)
obstructive lung dz (problem gettin air out)—> flow volume loop loops like a dinosaur
Where is the aorta and where is the IVC in this CT scan?
B= IVC (the bigger circular structure on the left/ patient’s right)
C= aorta (smaller circular structure on the right/ patient’s LEFT)
Kid passes out and dies on the football field from sudden cardiac death. What is the most likely cause of death and what 2 findings would you see on autopsy? (Describing this histo image is the answer to one of the things)
Hypertrophic (obstructive) cardiomyopathy (HCM, of the subtype HOCM)
1) massive myocyte hypertrophy (usually at the septum, making it hard for blood to get through from LV to aorta)
2) myocyte fiber disarray (irregular arrangement of myocytes with lots of connective tissue)
Order the speed of conduction of the following from fastest to slowest: atrial muscle, ventricular muscle, AV node, purkinje system
Purkinje system (fastest)—> atrial muscle—> ventricular muscle—> AV node (slowest bc it’s job is to slow speed of conduction from the SA node so the blood has sufficient time to fill)
We can do a screening test in which we take a sample of amniotic fluid to test if the baby’s lungs are healthy or will mostly likely be premature/ have surfactant deficiency. What does 1 and 2 represent in this graph?
1= lecithin (aka phosphatidylcholine) *this is a component of surfactant that should shoot up in late pregnancy
2= sphingomyelin
When a chest tube is placed (such as in pleural effusion), it is inserted at the 4th or 5th intercostal space around the mid-axillary line. What 3 muscles/ layers does the tube penetrate through?
Serratus Anterior Muscle, Intercostal muscles (external, internal, and innermost), and parietal pleura. The tube reaches the pleural cavity.
Which sections of the respiratory tree have cartilage and which ones do not?
The trachea and bronchus have cartilage. Bronchioles and beyond do not.
Which sections of the respiratory tree have cilia and which do not?
Trachea, bronchi, bronchioles, terminal bronchioles (the conducting zone) have cilia. The respiratory bronchioles and alveoli (the respiratory zone) does not have cilia.
Which sections of the respiratory tree have smooth muscle (and therefore could be affected by bronchoconstriction in asthma, for example)? Which do not?
Everything but the alveoli has smooth muscle (trachea, bronchi, bronchioles- terminally and respiratory)
College-aged student presents with low-grade fever and mild cough. Looking at the chest X-ray, what is the most likely cause of this patient’s symptoms?
Mycoplasma pneumoniae. This is the most common atypical pneumonia (esp. among college students/ military recruits in close quarters) of the interstitium, shown by incrased lung markings in the X-ray. (**other less likely atypical pneumonias: chlamydia pneumoniae, RSV, CMV, influenza virus, coxiella burnetti)
What does this look like?
Lobar pneumonia (conolidation or fluid of an entire lung lobe)
What category of pneumonia is this?
Bronchopneumonia= consolidation around the bronchioles (patchy). (Could be due to: staph A, H flu, pseudomonas, moraxella, or legionella.)
Why are chronic bronchitis patients described in textbooks as “blue bloaters”?
The excessive mucus from the chronic bronchitis plugs up the airways (mucus plugs) and traps CO2 (prevents it from getting out). Also prevents oxygen from getting in—> cyanosis—> “blue”
What histological finding is seen with A1AT (alpha-1 antitrypsin) deficiency?
PAS-positive globules in hepatocytes (PAS= type of staining and it’s in hepatocytes, or liver cells, because the mutated A1AT accumulates in the liver where it is made and cannot go out to the blood like it’s supposed to)
Construction worker/ plumber presents with fibrosis of the lung and the following histo slide is obtained from a lung sample. What is the most likely diagnosis?
Asbestosis (type of penumoconioses= interstitial fibrosis due to occupational exposure. Alveolar macrophages engulf particles—> fibrosis and restrictive lung disease/ trouble getting air in and expanding the lungs)
HISTO: shows Asbestos bodies
A shipyard worker is coughing and having a difficult time getting air in when taking a breath. What are you thinking?
Asbestosis (type of penumoconioses= interstitial fibrosis due to occupational exposure. Alveolar macrophages engulf particles—> fibrosis and restrictive lung disease/ trouble getting air in and expanding the lungs)
HISTO: shows Asbestos bodies
African American female presents with noncaseating granulomas in the lungs and hilar lymph nodes. She has also recently had vision problems, nodules on her skin, and says “doc, I can’t chew a cracker.” She is a teacher (no occupation that exposes her to chemicals). What is the most likely diagnosis?
Sarcoidosis
African American female presents with dyspnea, cough, elevated ACE, hypercalcemia. What is the diagnosis and proper treatment?
Sarcoidosis
Which chamber of the heart makes up most of the posterior side of the heart and resides adjacent to the esophagus?
The left atria (LA)
Which chamber of the heart makes up most of the posterior side of the heart and resides adjacent to the esophagus?
The left atria (LA)
What major vessel runs posterior to the LA and esophagus?
The descending thoracic aorta
*this means we can do transesophageal echo to detect aortic dissections and aneurysms
Explain the anatomical positioning of the ureteres in relationship to: the gonadal vessels, the internal/ external arteries, and the uterine artery.
What type of diuretic can be given to prevent calcium oxalate kidney stones?
Thiazide diuretics
(they inhibit the Na/Cl channel on the apical side, which dec Na brought into tubule cell—> stimulates Na/Ca channel on basolateral side to bring in more Na to cell to compensate—> this in turn inc Ca reabsorption so there’s more Ca in the blood, less in the urine capable of forming stones)
At what point will the murmur be loudest?
This is aortic stenosis (LV has to develop high pressures to pump blood out through stenotic aortic valve). So, you’ll hear a systolic murmur. It will be loudest at point B (not A) bc that’s the point where you have the greatest difference in pressures between the LV and aorta.
What are the 3 main inflammatory cells that play a role in the pathogenesis of COPD?
Neutrophils, macrophages (alveolar macrophages), and CD8+ cytotoxic T-cells.
These all release proteases as a byproduct of the inflammatory response, which contributes to alveolar destruction (so many proteases to deal with the gunk from smoking that there aren’t enough anti-proteases to balance out & protect the alveoli from damage). These proteases also play a role in the excessive mucus production (chronic bronchitis component).
Explain the concept of coronary steal. What drugs are capable of producing this effect?
When you have plaques in the coronary arteries, blood flow is limited so local vasodilators (adenosine, NO) will act to vasodilate so more blood can go through despite the plaques. If you get a pharm vasodilator (adenosine, dipyridamole), the vessels with plaques won’t be able to vasodilate any more, so the drug will only cause vasodilation to the vessels not occluded with plaques and they’ll steal away extra blood flow—> will make ischemic areas worse.
Fetal ultrasound reveals unilateral hydronephrosis. What is the most likely site of obstruction?
The ureteopelvic junction.
(hydronephrosis is dilation of the renal pelvis and calyces usually caused by obstruction)
Name the veins (with arrows).
Long-time smokers comes in with swollen right face and right arm. He also has swelling and engorgement of the veins in his right neck. Which vein is most likely obstructed?
The right Brachiocephalic vein. (Probably caused by a tumor pressing down on the vein)
Note: if this were SVC syndrome, the swelling in the face and arm would occur on both sides. Swelling occurs due to obstruction of the vein—> impaired drainage of blood—> backing up of blood.
A patient on loop diuretics starts popping in some ibuprofen (NSAID). His edema, which was well controlled with the diuretics, starts to come back more. What’s going on?
NSAIDs reduce the effectiveness of loop diuretics. Why? In addition to inhibiting the Na/K/Cl channel of the ascending loop of Henle, loop diuretics stimulate prostaglandin (PG) release (by unknown mechanism)—> inc renal blood flow and GFR= enhanced drug delivery. NSAIDs block the effect of PGs (they dec RPF, GFR), decreasing drug delivery to the loop of Henle, making loop diuretics less effective.
What do the following things do to the renal arteriole? Prostaglandins (PGs), Angiotensin II (ATII), NSAIDs, and ACE inhibitors.
Patient presents with shortness of breath, mild protein in urine and edema, and blood in urine. Based on that information and this IF, what is the diagnosis?
Goodpastures syndrome
Explain why you see “liner IF (immunofluroescence)” in Goodpastures. What does that even mean?
In Goodpastures, you have auto-antibodies against type 4 collagen. Since type 4 collagen makes up the BM (basement membrane) of blood vessels, the condition affects the ENTIRE glomerulus, so you have antibodies lining up along the blood vessel BM’s in a linear pattern and you see bright green all over this IF since it’s all affected (unlike other autoimmune conditions where antibodies only deposit in certain areas).
Is the bladder inside or outside of the peritoneum?
Outside. The bladder is extraperitoneal.
What must this be?
Atetlectasis (collapsed alveoli) from some type of brain hail obstruction, etc.
why? You can see tracheal deviation to the same side and this is the only thing that will cause tracheal deviation to the side of consolidation (the collapsed airways suck the pull the trachea like a vacuum sucking it to its side)
Explain the whole RAAS (the triggers, the goal of it, the pathway, the effects).
Diabetic patient. What med can you give to protect kidneys and prevent diabetic nephropathy (especially if they are hypertensive or are showing signs of decreased renal function)?
ACE inhibitor or ARB
they decrease GFR (and improve renal blood flow) to take the pressure off the kidneys
If you give a beta-blocker, which part of the EKG will be changed?
B (the PR interval).
Beta-blockers PROLONG the PR interval. (They block the beta-1 receptors on cardiac pacemaker cells—> slower influx of Na+—> will take longer for depolarization to happen).
*Remember: longer PR interval= takes longer for electrical signal to travel from SA node in atria—> AV node to ventricles and to bundle of His and fasicular branches
Male comes in peeing out blood, flank pain on left side. CT shows compression of left renal vein between the aorta and SMA (superior mesenteric artery). What vascular problem is most likely to result from this?
Varicocele (varicose veins in th testes “bag of worms”)
You’re a surgeon doing a kidney transplant. Which kidney (right or left) are you going to take out of the patient and replace and why?
Left. The left renal vein is longer, so there’s longer veins/ more space to work with.
Which varicocele is more common (right or left)? Which is more concerning? Why?
Left-sided varicocele is far more common. It is due to obstruction/ compression of the left renal vein between the aorta and SMA—> fluid backs up in the left kidney and down into the left testicular vein because it cannot drain forward (due to obstruction/ compression)—> varicose veins in left testicle.
Right-side varicocele is more concerning because that means there’s obstruction/ compression over the IVC.
What is a varicocele? Explain the pathophysiology of a left-sided varicocele in a man.
Varicocele= variocse veins (“bag of worms”) in the testes.
Tumor/ obstruction/ compression of left renal vein between the aorta and the SMA (superior mesenteric artery)—> backing up of fluid that should be draining forward to the heart, backs up into left kidney and left testicular vein—> back flow of fluid in veins= leaky valves= varicose veins= left-sided varicocele.
Which part of the nephron is impermeable to water regardless of ADH levels?
The ascending loop of Henle and the early DCT.
Patient has severe HTN with end-organ damage. What type of arteriosclerosis is this?
Hyperplastic arteriOLOsclerosis
(Malignant HTN—> thickening of vessel wall by hyperplasia of smooth muscle) **notice “onion-skinning” appearance of the vessel smooth muscle
Patient has diabetes and HTN. What type of arteriosclerosis is this?
Hyaline arteriOLOsclerosis
(diabetes or long-standing BENIGN HTN—> chronic endothelial injury from hyperglycemia or high pressure on the vessel walls—> proteins in the bloodstream leak into the damaged vessel wall intima and media layers—> lay down eosinophilic hyaline membrane) *think of it like scarring/ like a plaque
Name the main autonomic receptors to know that act through GPCRs and what type of mechanism they have (Gq, Gi, or Gs)
Mnemonic: “After kisses (quisss) you get a kick (qiq) out of sick (siq) super qinky sex (sqs)”
Draw out the autonomic receptors flow chart.
Explain the different GPCR pathways: Gq, Gs, and Gi.
What are the drug classes (in order) we give to asthma patients? COPD patients? What suffix do these drug classes end in so you can recognize them?
*You give asthma patients an ICS first because asthma is more of an inflammatory process.
Mnemonic: “Arnold Schwarzenegger (ICSteroid) thinks he’s #1 (end in -one). Then there’s the lab dog (LABA, ends in -ol). Then there’s the lamb (LABA) and they are slow so think “i’m late” (end in -ium and -late).
Explain treatment in asthma and COPD, including what receptors the drug classes act on and the suffixes of the drugs that would fall in the classes. Also, why can a beta-blocker be harmful to a patient with asthma or COPD?
What is the order of renal blood flow?
Renal artery—> segmental artery—> interlobar artery—> arcuate artery—> interlobUlar artery—> afferent arteriole—> glomerulus—> efferent arteriole—> vasa rectua/ peritubular capillaries—> venous outflow.
What is the flow of urine (starting from the kidneys all the way out—be specific)?
Medullary pyramids—> renal papillae—> minor calyx—> major calyx—> renal pelvis—> ureter—> bladder—> urethra
What are the 3 layers of the glomerular filtration barrier?
Explain this graph.
As you inc GFR, you are filtering through more Cr, so Cr in the blood goes down.
Describe the picture of the nephron and where each class of diuretics act (what segment of the nephron and what channel).
Fetal circulation:
Most of the Oxygenated blood reaching the heart through the _____ is directed through the _____.
Most of the DEOXYGENATED blood from the _____ passes through the __(explain)___.
Most of the Oxygenated blood reaching the heart through the IVC is directed through the foramen ovale (RA—> LA, bypasses lungs). Remember: Oxygenated blood (coming up from IVC bc of its connection to the umbilical vein) goes through foramen Ovale.
Most of the DEOXYENGATED blood from the SVC passes through the RA—> RV—> main pulm artery—> ductus arteriosis—> descending aorta (bypasses lungs at a later point).
You see ST elevations in leads II, III, and aVF. Which coronary artery is occluding causing the MI? Which part of the heart had blood flow cut off to it?
RCA (right coronary artery)
SA node
Name all the blacked-out parts of this Wigger diagram.
Which PV loop represents changes that occur to the heart when a nitrate is given to treat angina/ MI/ HF?
E (decreases preload and afterload)
What does this curve represent? Which line—top or bottom—would correspond to emphysema? How about fibrosis?
Lung compliance (C= change in volume/ change in pressure).
Top= emphysema- inc compliance (stretchy lungs, obstructive, hard to empty)
Bottom= fibrosis- dec compliance (stiff lungs, restrictive, hard to fill)
What heart chamber makes up most of the heart’s anterior surface? What heart chamber makes up most of the heart’s posterior surface? What chamber cannot be seen at all from the anterior side?
Anterior- RV
Posterior- LV
Cannot be seen from anterior side- LA
Patient who recently got into a car crash comes to the ED and develops worsening shortness of breath and confusion and has scattered petechial rash on thorax. He dies and biopsy of vessels reveals this. What probably happened to him from the car crash?
Fracture of long bone or pelvis—> fat emboli
(presents with triad: hypoxemia, neurological abnormalities, and petechial rash)
When presented with an acid/base question, what are the 4 steps for tackling the problem to figure out the acid-base status of the patient and if their body is compensating appropriately?
In acidosis, renal ammoniagenesis is stimulated. This process is responsible for the majority of renal acid excretion in chronic acidotic states. What is this process and what amino acid is involved?
Tubular epithelial cells metabolize glutamine—> glutamate to make ammonium (NH3) excreted in urine (get rid of acid) and bicarb reabsorbed into blood (hold onto base).
Explain stress urinary incontinence. (What it is, what can cause it, how we diagnose it, what we can do about it)
Explain urgency urinary incontinence. (What it is, what can cause it, what we can do about it)
Explain overflow urinary incontinence. (What it is, what can cause it, how we diagnose it, what we can do about it)
Older adult presents with gross painless hematuria. What is the most likely diagnosis?
Clear cell carcinoma.
gross, painless hematuria in older adults is urinary tract cancer (urothelial CA or Renal Cell Carcinoma) until proven otherwise. The most common type of RCC is clear cell carcinoma (that was also a histo image of it).
In what condition do you see this EKG pattern and why?
Wolff-Parkinson-White (WPW) syndrome.
This is a ventricular pre-excitation syndrome. The electric signal goes through an accessory “secret pathway,” bypassing the rate-slowing AV node—> ventricles get depolarized before they should.
How can BPH affect a man’s ability to urinate? How can it progress to affect the kidneys?
Enlarged prostate presses on the urethra. At first it’s hard to get pee out (will have to strain to urinate). As it progresses, incomplete emptying of the bladder can progress to overflow incontinence (you don’t get all the pee out when you go—> some urine will leak out throughout the day when pressure in the bladder overcomes the sphincters). The high pressure in the bladder can back up to the ureters and kidney (hydronephrosis) and can even progress to acute kidney injury (AKI).
Draw the diagram of alveoli in inspiration, no air flow, and expiration and example values of Alveolar pressure, pleural pressure, and transmural pressure (what’s the equation for it?).
At the red point, what is the approximate pleural pressure going to be?
The red point shows the FRC (functional residual capacity, or the amount of air in your lungs after breathing out normally). After exhalation, your pleural pressure is -5.
*note: the transmural pressure is always positive, meaning the force of the lungs pulls inward and the pleural pressure is always negative, meaning the chest wall pushes outward (only exception to this is when the lungs are collapsed).
ST elevations in leads I and avL. Which coronary vessel was occluded leading to the MI?
left circumflex (LCX)
ST elevations in leads II, III, and avF. Which coronary vessel was occluded leading to the MI?
Right coronary artery (RCA)
ST elevations in leads V1-V6. Which coronary vessel was occluded leading to the MI?
the LAD (lateral descending artery)
ST elevations in leads V7-V9 and ST depressions in V1-V3 with tall R waves. Which coronary artery was occluded leading to this MI? Where does it branch from?
The PDA (posterior descending artery).
if right dominant—> PDA branches off RCA
if left dominant—> PDA branches off LCX
if co-dominant—> PDA branches off both RCA and LCX
What blood vessel supplies the top of the ureters? What blood vessel supplies the bottom of the ureters?
Top ureters are supplied by branches of the renal artery. Bottom ureters are supplied by the vesical artery.
*note: a complication of renal transplantation is ischemia to the lower ureters (where vesical artery supplies) due to lack of connections—> urine leakage in the body
What are the major side effects of the class III anti-arrythmic drug Amiodarone? (Categories: cardiac, pulmonary, endocrine, GI/ hepatic, ocular, derm, and neurologic)
Patient has a history of rheumatic fever and now presents with a diastolic murmur. What is the valvular disorder and where is the murmur heard loudest?
Mitral stenosis (note that mitral regurgitation is most common post-rheumatic fever, but can progress to mitral stenosis and we know it’s stenosis in this case bc it’s a DIASTOLIC murmur).
Heard loudest at C (mitral valve OPENS bc stenosis= problem opening the valve).
Asian kid <5 years presents with conjunctival injection (red, bloodshot eyes), rash, adenopathy (swollen cervical lymph nodes), strawberry tongue, edema in the feet, and fever. What are you thinking?
Kawasaki disease (medium-vessel vasculitis)
Mnemonic: “CRASH and burn”
Conjunctival injection, Rash, Adenopathy (cervical), Strawberry tongue, and Hand/ feet edema and redness and fever.
*note: presents similarly to group A Strep (rash, strawberry tongue), but conjunctivitis, swollen hands/ feet, and persistent high-grade fever suggest Kawasaki. Also, Q stem will be an Asian kid <5 y.o.
Kids with Kawasaki disease are at highest risk for what heart problems?
Coronary artery aneurysms, thrombosis, or rupture. Can have MI’s and sudden death as a result. (Remember our doctoring case study was a kid with Kawaskis in need of a heart transplant)
In kids, aspirin is usually contraindicated due to the risk of Reye’s syndrome. However, in a particular medium-vessel vasculitis, aspirin should be given. What condition is this where you’d want to treat with aspirin (and IV Ig)?
Kawasaki disease
What are the gross changes to the heart, microscopic changes to the heart, and complications most likely to occur after a heart attack within: <4 hrs post-MI, 4-24 hrs, 1-3 days, 4-7 days, 1-3 weeks**, and after **months?
A blood clot travels and occludes the artery of the eye causing blindness. What’s the course of travel of the blood clot (3 vessels)?
internal carotid—> ophthalmic artery—> retinal artery
Releases of the hormones ANP (from atria) and BNP (from ventricles) will have what 3 effects on the ventricles?
1) inc GFR
2) dec Na+ reabsorption in the PCT
3) dec Renin levels
Why? The goal of these hormones is to dec BP (opposite of Aldosterone and the RAAS) back to normal levels when there is too much fluid volume filling up the ventricles/ too high of BP
On X-ray, what does “thumbprint sign” suggest? How about “steeple sign”?
Thumbprint sign—> epiglottitis (think H. Flu)
Steeple sign—> croup (think Parainfluenza)
Tall thin guy with a 1 year smoking pack year history was sitting on the couch and all of the sudden got right-sided chest pain and trouble breathing. Diagnosis?
Primary spontaneous pneumothorax (rupture of apical subpleural blebs—> collapsed lung)
(risk factors: tall, skinny guys in their 20s bc weight of the lungs pulls down and smoking)
Football player gets tackled and breaks his 12th left rib. What organ is most likely to get punctured by the broken rib?
The left kidney.
Fill in the blanks of this electrolyte panel.
Where is the AV node located?
In the RA above the tricuspid valve, near the interatrial septum and opening of the coronary sinus (which drains into the RA)
A patient becomes very hypotensive and tachycardic after a high-speed vehicle accident, then dies. Which part of the patinet’s Aorta was probably damaged?
C. The aortic isthmus
(This patient had a blunt aortic injury, meaning a traumatic aortic rupture. This part is tethered by the ligamentum arteriosum and is more fixed than other parts of the thoracic aorta, and therefore more likely to rupture from trauma.)
How do calcifications develop in older people with aortic stenosis?
Early stages of aortic stenosis mimic atherosclerosis, but in the aortic valve. Later on, valve fibroblasts differentiate into osteoBlast-like cells and deposit bone matrix, or calcifications
