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Advanced Pathophysiology > Exam 5 Study Guide > Flashcards

Exam 5 Study Guide Flashcards

1
Q

What is nephrolithiasis?

A

Also known as kidney stones or renal calculi. This is the presence of renal stones in the renal pelvis and are made of calcium, struvite, uric acid, or cystine.

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2
Q

What are calcium stones? Explain.

A

They are the most common type of kidney stones. They typically occur from idiopathic hypercalciuria or in the setting of hyperparathyroidism because this causes an increase in osteoclast activity which are the bone cells that break down bone and release calcium into the blood.

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3
Q

What are struvite stones? Explain.

A

They are the second most common type of kidney stones and are made of magnesium, ammonium, and phosphate salts.
They result from chronic UTIs with urease-producing bacteria which break down the urea in the urine to salts that compose the struvite stones.
They cause intractable UTIs, pain, bleeding, and abscesses.

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4
Q

What are uric acid stones? Explain.

A

They are the third most common type of kidney stones and result from a breakdown of purine. These types of stones tend to form in those with excess purine intake or those with gout.

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5
Q

What are cystine stones? Explain.

A

They are the least common type and occur more in children.

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6
Q

What is the pathogenesis of nephrolithiasis?

A

This occurs due to an oversaturation of the urine with ions. The cations and anions bond with one another and form salts which turn into crystals. These crystals then form the stones that pass the ureter and cause excruciating flank pain and obstruction. This obstruction causes the urine to back up into the kidneys causing hydronephrosis and renal failure.

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7
Q

What are the risk factors for nephrolithiasis?

A
  1. gout which causes the accumulation of uric acid
  2. high protein diets resulting in increased purine intake
  3. high sodium diet resulting in increased calcium excretion and therefore calcium stone formation
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8
Q

What are the clinical manifestations of nephrolithiasis?

A
  1. flank pain that radiates to the groin (renal colic)
  2. anuria and hematuria
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9
Q

What are the 3 stages of AKI?

A

Stage 1: Creatinine of 1.5-1.9x higher than the baseline
Stage 2: Creatinine of 2-2.9x higher than the baseline
Stage 3: Creatinine of 3x higher than baseline or in those <18 years of age, a decrease in GFR to <35 ml/min

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10
Q

What is a normal GFR level?

A

90-120 ml/min

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11
Q

What is pre-renal AKI?

A

Caused by impaired blood flow to the kidney or decreased renal perfusion resulting in a decreased GFR.

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12
Q

What are the causes of pre-renal AKI?

A

1.vasoconstriction/hypotension/hypovolemia
2. renal artery stenosis
3. heart failure due to inadequate cardiac output

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13
Q

What is the main cause of intra-renal AKI?

A

Acute tubular necrosis because it is impairing renal function at the cellular level of the kidneys

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14
Q

What is acute tubular necrosis?

A

A severe necrosis of tubular epithelial cells. The cells slough off and collect in the tubule, causing obstruction which leads to increasing tubular pressure and decreased GFR. This causes the arteriole to vasoconstrict and leads to backflow of fluid into the renal interstitial tissue. This will all lead to rising BUN and creatinine which will peak and then come back down. As it comes back down, patients will diurese and become severely dehydrated.

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15
Q

What can you see in a UA with those with acute tubular necrosis?

A

muddy brown cast cells

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16
Q

What occurs in post-renal AKI?

A

Caused by any obstruction such as bladder outlet obstruction which can occur as a result of prostatic hyperplasia or uretral obstruction from a kidney stone.

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17
Q

What are the clinical manifestations of AKI?

A
  1. oliguria, anuria
  2. electrolyte imbalances including hyperkalemia and hyponatremia
  3. metabolic acidosiss
  4. BUN: Creatinine ratio will be >20 in a pre-renal AKI and normal in intra-renal AKI
  5. FeNa will be <1% in pre-renal AKI and >2% in an intra renal AKI
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18
Q

What is FeNa?

A

Fractional excretion of sodium that is used to evaluate AKI and to differentiate between pre-renal and acute tubular necrosis.

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19
Q

What does FeNa <1% indicate?

A

Indicates pre-renal AKI and that the kidneys are conserving sodium

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20
Q

What does FeNa >2% indicate?

A

Kidneys are wasting sodium which indicates acute tubular necrosis

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21
Q

What does a BUN: Creatinine ratio indicate?

A

BUN: creatinine ratio >20 is consistent with pre-renal AKI

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22
Q

What are the stages of CKD?

A

Stage 1: GFR >90: Patients are asymptomatic
Stage 2: GFR 60-80: Patients experience an increase in PTH, early bone disease, and increasing creatinine and urea.
Stage 3: GFR 30-59. They will have erythropoietin deficiency, anemia, and an increase in creatinine and urea. They will have mild HTN.
Stage 4: GFR of 15-29. These patients will have increased triglycerides, metabolic acidosis, hyperkalemia, and elevated BUN/creatinine.
Stage 5: GFR <15 or need for dialysis. This results in uremia, severe HTN, anemia, and hyperphosphatemia.

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23
Q

What are the most common causes of CKD?

A

diabetes, HTN, and glomerulonephritis

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24
Q

What is pathogenesis of CKD?

A

chronic injury to kidneys which causes irreversible loss of nephrons and causes an increase in glomerular filtration pressure in the remaining nephrons. this causes more nephrons to fibrose and scar.

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25
Q

What are CM of CKD?

A
  1. uremia: accumulation of urea and other toxins which accumulate due to a decrease in GFR/renal function
  2. anemia secondary to decreased erythropoietin levels which can lead to left ventricular hypertrophy
  3. hypernatremia and hyperkalemia occur in the later stages as pt become oliguric and cannot excrete the electrolytes
  4. hyponatremia occurs in early stages secondary to lack of kidney’s ability to concentrate urine
  5. metabolic acidosis occurs because of the kidneys inability to rebasorb urinary bicarb or excrete H+.
  6. hyperparathyroidism occurs due to hypocalcemia which is secondary to hyperphosphatemia.
  7. osteodystrophy occurs from secondary hyperparathyrodisim
  8. insulin resistance occurs due to hyperparathyroidism decreasing insulin sensitivity. as kidney function decreases, it cannot clear adiponectin and leptin which contribute to insulin resistance
26
Q

What is polycystic kidney disease and what are side effects of it?

A

autosomal dominant disorder which produces a defect in the formation of epithelial cells and causes cysts and obstruction of renal parenchyma, fibrosis, and loss of functioning neurons.

HTN, valvular disease, and cerebral/aortic aneurysms can occur

27
Q

What is hemolytic uremic syndrome?

A

occurs due to e coli strain found in animals, unpasteurized beverages, or contaminated foods. characterized by hemolytic anemia, thrombocytopenia, and renal impairment. most common AKI in children.

28
Q

What is the pathogenesis of HUS?

A

shiga toxin which is found in e coli is absorbed into the blood and is transported to the kidneys where it causes breakdown and separation of glomerular capillary endothelial cells from the basement membrane, and activation of platelets and coagulation cascade. platelets and fibrin clots occlude the glomerular arterioles which then swell causing RBCs to be damaged and fragment. The fragments are removed by the spleen and the child will then experience hemolytic anemia and experience renal failure

29
Q

What occurs in D+ HUS?

A

this is hemolytic anemia that occurs after 1-2 weeks of a GI illness. the child may be symptom-free for 1-5 days after the illness and then will suddenly experience pallor, bruising, and oliguria. renal failure can occur 2 days-2 weeks after the onset of symptoms

30
Q

What is cholelithiasis?

A

presences of stones in the gallbladder which are made of bile, cholesterol, and bilirubin

31
Q

What are risk factors of cholelithiasis?

A

oral contraceptives
native american ancestry
high triglycerides
obesity due to increased cholesterol in bile
females due to the estrogen which reduces bile acid synthesis and increases liver secretion of cholesterol into bile
malabsorption increases risk because it interferes with absorption of bile salts which are needed to maintain solubility of cholesterol and can increase risk of stones

32
Q

what is a hallmark sign of cholelithiasis?

A

biliary colic which is a sharp and abrupt pain in the RUQ or epigastric area. the pain increases in intensity and then levels off in 30-60 minutes and will last until there is no more food stimulating gallbladder contraction

33
Q

What is cholecystitis?

A

inflammation of the gallbladder due to an obstruction in the biliary tract and is associated with cholelithiasis. the gallstones are made of concentrated bile which causes chemical irritation of the inner wall of the gallbladder and is a prime condition for bacterial growth

34
Q

What are CM of cholecystitis?

A

Positive Murphy’s sign and is precipitated by a fatty meal because the increased fat increases the need for bile to emulsify fat and secretion of bile puts a strain on the already inflamed gallbladder and causes pain

35
Q

What are lab abnormalities of cholecystitis?

A

leukocytosis, increased ALP, and increased direct bilirubin levels

36
Q

What is appendicitis?

A

Inflammation of the appendix which usually occurs between ages 10-19.

37
Q

What is the major CM of appendicitis?

A

Pain that initially may be epigastric or periumbilical but then settles in the RLQ.

38
Q

What is diverticular disease?

A

Diverticula in the large intestine that are outpouchings of mucosa from the muscle layer of the intestine that protrude into the intestinal lumen

39
Q

What is the difference between diverticulosis vs diverticulitis?

A

Diverticulosis is the presence of diverticula in an asymptomatic individual and diverticulitis is inflammation of the diverticula

40
Q

What is a major CM of diverticulitis?

A

Results in LLQ pain

41
Q

What is ulcerative colitis?

A

Inflammatory disease of the large intestine which commonly affects the rectum and colon and has periods of remission and exacerbation.

42
Q

What are CM of UC?

A
  1. chronic recurrent diarrhea and bloody stools
  2. severe ulcerations of the large intestine which begin in the rectum and may involve the entire large intestine
  3. Not transmural, it remains superficial
43
Q

What are those with UC at more risk of?

A

They are at increased risk of VTE and microthrombi from the chronic inflammation they experience

44
Q

What are the two types of inflammatory bowel disease?

A

Crohn’s Disease and UC

45
Q

What is Crohn’s Disease?

A

chronic inflammatory disorder of GI tract where the entire wall (transmural) of the intestine is affected and there is a presence of skip lesions (areas of healthy tissue surrounded by diseased tissue which are randomly present)

46
Q

What are risk factors of Crohn’s disease?

A
  1. family history
  2. jewish descent
  3. the CARD 15/NOD 2 gene mutation
  4. impaired t cell immunity
47
Q

How does the CARD 15/NOD 2 gene mutation affect those with Crohn’s?

A

the gene encodes for a protein which is involved in the recognition of bacterial wall fragments in the intestinal epithelial cells. a genetic mutation here imapirs these cells from identifying bacteria

48
Q

What are CM of Crohn’s disease?

A
  1. fistulas (abnormal tracts that develop in presence of inflammation) and strictures can form from fistulas between the intestines, bladder, and vagina
  2. abdominal pain
  3. bloody stools
  4. malabsorption which can cause vitamin deficiences
49
Q

What is stress related mucosal disease?

A

they are stress ulcers often associated with those who are critically ill and they have 2 classifications- ischemic or cushing

50
Q

What is the primary manifestation of SRMD?

A

GI bleeding

51
Q

What are ischemic ulcers?

A

they occur within hours of an event which has led to gastric ischemia such as hemorrhage, burns, heart failure, or sepsis

52
Q

What are cushing ulcers?

A

they are stress ulcers that occur as a result of TBI or brain surgery

53
Q

What is peptic ulcer disease?

A

break in integrity of mucosa of upper GI tract which causes it to be exposed to gastric acid which causes ulcerations

54
Q

at what levels can you visually see jaundice?

A

when bilirubin levels reach 2.5-3 (normal bilirubin levels are <0.3)

55
Q

what is non obstructive jaundice?

A

also known as indirect or unconjugated bilirubin which is usually from RBC hemolysis. there is more bilirubin produced then can be conjugated by the liver so this results in excess unconjugated bilirubin in the blood.

56
Q

what is obstructive jaundice?

A

occurs when the liver can conjugate bilirubin without issues but there is an obstruction in the outward flow of bilirubin to the intestines from the liver , usually caused by an obstruction of the biliary tract.

57
Q

what is a hallmark sign of obstructive jaundice?

A

gray stools because bilirubin is what give stools their brown color

58
Q

what are clinical manifestations of acute pancreatitis?

A

epigastric pain that radiates to the back
hypovolemic shock (low BP, tachycardia, cool, clammy skin)

59
Q

what are risk factors to esophageal cancer?

A

barrets esophagus and chronic exposure to irritants

60
Q

what is a major side effect of neonatal jaundice?

A

unconjugated bilirubin can cross the blood brain barrier in infants and cause bilirubin encephalopathy (kernicterus) from bilirubin being deposted in the brain cells

Advanced Pathophysiology (22 decks)

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