Shortly after a routine pernatal checkup, Neko’s ob-gyn ordered a set of tests of the fetal heart. The doctor told her she suspects that the fetus likely has transposition of the great arteries. The doctor was too busy to explain this problem to Neko. Describe normal flow through the heart and how flow through the heart would change with this condition. Is this a cyanotic or non cyanotic congenital defect in the infant? Would it also be cyanotic in the fetus? Why or why not?
Normal flow: inf/sup vena cava –> RA –> bicuspid valve –> RV —> pulmonary semilunar valve –> pulmonary arteries -> lungs –> pulmonary veins –> LA –> mitral valve –> LV –> Aortic semilunar valve –> arterties to systemic circulation
With transposition of the great arteries, the pulmonary arteries and systemic arteries are affected. Two circulations are formed. The right side of the heart forms its own circulation while the left does the same. This is cyanotic in the infant because the oxygenated blood never circulates systemically. The fetus doesn’t depend on their lungs due to the foramen ovale and umbilical supply with the mother. This is however an issue at birth.
Is aortic semilunar stenosis a systolic or diastolic dysfunction? What would be the effect on cardiac output? Which chambers of the heart would be affected form this aortic semilunar stenosis and how would they be affected?
Aortic semilunar stenosis is a systolic dysfunction that decreases cardiac output. The left ventricle pressure is increased due to the decreased stroke volume due to the difficulty vacating the ventricle. The heart rate is increased by the body in an attempt to help, however, this only increases the work on the heart, increases pressure and decreases Q even more, eventually leading to ventricular hypertrophy.
What are three cardiomyopathies and their effects on cardiac output, myocardium thickness, and chamber volume?
Dilated: Decreased Q, decreased myocardium thickness, increased chamber volume
Hypertrophic: Decreased Q, increased myocardium thickness, decreased chamber volume
Restrictive: decreased Q, increased myocardium thickness, decreased chamber volume
Contrast the signs and symptoms of nephrotic and nephritic syndrome
Nephrotic: increased glomerular permeability
- massive proteinuria
- hyperlipiduria and hyperlipidemia
- Na+ retention to compensate for increased fluid loss
- hypoalbuminemia
- ascites
Nephritic: immune related
- Includes Berger and Goodpasture’s disease
- hematuria
- casts (RBC’s and WBC’s)
- proteinuria
- inflammation
- hypertension
What are three aspects of ECG interpretation that are used to detect arrhythmias?
Rate - heart rate
Rhythm - sounds between S1 –> S3
Presence - is it there?
Size and Shape
Katherine had a wild weekend and tried cocaine with some friends. A few days later she was hospitalized with renal failure. While visiting her, she expressed she was glad it was just her kidneys that were harmed and nothing else. Explain to her why kidney failure might lead to dysfunction of other body systems and give 3 examples of effects on 3 different organ systems.
Kidneys are in charge of excreting toxins and play a major role in homeostasis
- Kidneys release erythropoetin and without it, there will be a decrease in RBCs through the role of erythropoetin in the formation of RBC in bone marrow (anemia)
- Edema increases blood pressure and volume and puts strain on the heart that can ulitmately lead to cardiac failure.
- Harder time excreting H+ ions and putting the body in a state of acidosis will increase pulmonary breathing rate to compensate
Kurt walked into a urologist complaining of infrequent urination. A CT scan confirms that he has stenosis of the renal arteries limiting blood flow to both kidneys. Describe which type of acute renal failure he is suffering from. How will this affect filtration pressure in the glomerulus (address both pressure in the capillary and in the Bowman’s capsule). What would be the expected effect on the BUN:creatine ratio and why?
Kurt is suffering from prerenal failure. The filtration pressure in the capillary will be decreased due to decreased blood pressure in the kidneys. The Bowman’s capsule should still be normal. The expected BUN:creatine ratio would be > 20:1 because aldosterone and angiotensin 2 will have caused the kidneys to reabsorb water and solutes from the blood to try and increase blood pressure.
Buster had a myocardial infarction. After he was diagnosed with atherosclerosis he is wondering if there is anything he can do different to decrease his risk of another myocardial infarction. What are two risk factors for atherosclerosis that he could change to decrease the risk?
- Hyperlipidemia: needs to decrease fat intake (especially cholesterol)
- Obesity and sedentary lifestyle: needs to increase physical activity
What are potential causes of hyponatremia? What signs and symptoms would be expected?
Causes: decreased serum Na+, increased serum H2O by
- Heart failure: decreased forward flow from the heart causes kidneys to increase what they perceive as low intravascular volume by RAAS so volume is increased and Na+ is decreased, perceived low volume activates ADH to further H2O retention
- Cirrhosis decreases blood seen by kidneys so reabsorption due to perceived low volume increases, urine sodium decreases, but water reabsorption > Na+ reabsorption
- Primary polydipsia (excess water consumption) increases plasma volume but sodium remains the same
- SIADH
- Hyperaldosteronism
- Emesis/diarrhea
Signs and symptoms would include neuron swelling, fatigue, nausea,
What is the expected difference in the BUN:creatine ratio in prerenal compared to intrarenal failure? Why?
In prerenal failure, BUN;creatine > 20/1 because the body is going to try and reabsorb all the solutes and water in an attempt to raise filtration pressure by means of aldosterone and angiotensin II.
Intrarenal failure has BUN:creatine at normal 20/1 levels because the damaged nephrotic cells are not able to respond to aldosterone and angiotensin II
Carl and Dan walk into a urologist both complaining of infrequent urination. Carl is diagnosed with a bladder stone, and Dan has a thrombus blocking his renal artery. Describe which types of acute renal failure each is suffering from. Would you expect their BUN and serum creatinine to be similar? Why or why not? Contrast the effect of both of these conditions on filtration pressure in the glomerulus (pressure in the capillary vs. the pressure in the Bowman’s capsule)
Carl is suffering from postrenal failure, while Dan is suffering from prerenal failure. Carl’s BUN:creatine levels should be normal while Dan’s are going to be elevated due to the body trying to increase renal pressure by reabsorbing all solutes and water by means of aldosterone and angiotensin II. Carl’s glomerular filtration pressure should be normal but his Bowman’s capsule pressure will be elevated due to back pressure on it caused by the blockage in the bladder. Dan’s glomerular filtration pressure is going to decrease due to the decrease in the arterial pressure but his Bowman’s capsule pressure should remain normal.
What are the effects of Angiotensin II secretion on the body? What would be the effect of taking an ACE inhibitor on blood pressure? Why?
Angiotensin II’s main effect is to constrict blood vessels and increase blood pressure. ACE inhibitors block the body’s production of angiotensin II, prevents constriction, lowers blood pressure, and causes heart to use less energy from beat to beat.
How does the body compensate for fluid loss and pH change after excessive vomiting?
- Increase ADH which Increases RAAS that causes Increased Na+ and H2O reabsorption and H+ secretion causes increased H+ in urine
- Loss of Cl- causes Increased HCO3- reabsorption
- Loss of H+ by vomiting would cause alkalosis in the serum. When HCO3- makes it to the kidneys, they realize there is a more negative charge, so secrete K+ in urine and H+ goes into cells
- Body would compensate for increase in pH by hypoventilation and which would increase CO2
