Exam 5 Final Guide Questions Flashcards

1
Q

What is the difference between oncotic pressure and hydrostatic pressure and how do they contribute to ascites?

A

Hydrostatic pressure exceeds oncotic pressure which leads to ascites. Hydrostatic pressure will force fluid out into the intersitial tissue leading to edema and ascites.

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2
Q

What happens to PTH in CKD?

A

In CKD, the kidneys are unable to ‘activate’ vitamin D so less calcium is absorbed and blood calcium levels fall. This triggers the parathyroid glands to overproduce PTH in an attempt to increase the amount of calcium in the blood. This leads to secondary parahyperthyroidism which then leads to osteodystrophy and insulin resistance

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3
Q

What are characteristics of struvite renal stones?

A

They are the second most common type of kidney stone and are made of magnesium, ammonium, and phophate salts.
They tend to result from chronic UTIs with urease producing bacteria such as proteus and pseudomonas. The ureas produced by these bacteria break down the urine to the salts that comprosie the struvite stones

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4
Q

What is the end product of protein metabolism?

A

Amino acids are the end product of protein metabolism in humans. When proteins and amino acids are broken down in the body, ammonium is created as a byproduct. Ammonium is dangerous when it remains free in the human body, so something must be done to get rid of it. The major route of removal of ammonium by the body is via urea synthesis in the liver.

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5
Q

What do most testicular cancers secrete?

A

AFP. Alpha fetoprotein in non-pregnant people is mainly measured as a tumor marker. Tumor markers are substances that are often made by cancer cells or by normal cells in response to cancer. High levels of AFP can be a sign of cancer of the liver, ovaries or testicles.

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6
Q

What are causes of hepatic encephalopathy?

A
  1. Accumulation of ammonia
  2. GI bleed (breakdown of bleed leats of large protein load–> large ammounts of ammonia)
  3. portal vein thrombosis
  4. medications with sedating effects
  5. hyponatremia
  6. diabetes in an individual with Hepatitis C
  7. CKD
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7
Q

What are causes of acute tubular necrosis?

A

Any type of ischemia to the renal tubules at the cellular level can cause ATN

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8
Q

What are characteristics of ATN seen in a UA?

A

Muddy brown cast cells are seen in the UA of a patient with ATN

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9
Q

How does portal hypertension bleeding most commonly occur?

A

from esophageal variceal bleeds

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10
Q

What is the pathophysiology behind alcholic cirrhosis?

A

fatty liver occurs due to hepatic fat accumulation
Alcohol -> acetaldehyde -> liver fibrosis
Mitochondrial fx is impaired decreasing oxidation of fatty acids
Acetaldehyde inhibits export of proteins

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11
Q

What are signs and symptoms of duodenal ulcers?

A

melena and hematemesis due to it being an “upper GI bleed” located in the duodenum

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12
Q

What is the first sign of small bowel obstruction?

A

Distention which decreases the intestines ability to absorb water/electrolytes and increased secretions of these things into the lumen which lead to fluid accumulation and gas. This is important to understand because those with SBO need to have their electrolytes/fluids monitored so that they dont become dehydrated

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13
Q

What are signs and symptoms of SBO?

A
  1. Hypokalemia due to electrolyte/fluids loss which also causes hypovolemic shock symptoms
  2. distention
  3. colicky abdominal pain
  4. metabolic alkalosis from hydrogen ion loss secondary to vomiting
  5. obstruction of the pylorus results in profuse vomiting of clear gastric fluid
  6. a partial SBO results in diarrhea while a complete SBO results in constipation
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14
Q

Where do peptic ulcers occur?

A

In the duodenum which includes both gastric and duodenal ulcers

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15
Q

What type of pain occurs with gastric ulcers?

A

The epigastric pain is worse when eating and pain is immediate

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16
Q

What is the age group of those get Crohn’s disase?

A

Crohn’s is usually diagnosed in young adults between the ages of 15-35

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17
Q

what are signs and symptoms of chron’s disease?

A
  1. skip lesions
  2. malabsorption which causes vitamin deficiencies in B12, vitamin D, calcium, and folic acid
  3. fistulas (abnormal tracts that develop in the presence of inflammation) which can cause strictures between the intestines, bladder, and vagina
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18
Q

What will screening look like in those with an acute hepatitis B infection?

A

Acute infection is present when both the hepatitis B core antibody (IgM) and the hepatitis B surface antigen are positive

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19
Q

What will screening look like in those with chronic hepatitis B infection?

A

chronic infections are present when both the total core antibody and the hepatitis B surface antigen are present

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20
Q

What are prevention methods for hepatitis A?

A

Handwashing and Hep A vaccine is available to prevent this

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21
Q

How is Hepatitis C transmitted?

A

transimtted through blood, body fluids, tattoos, and IV drug use

22
Q

What is the pathophysiology of cholelithiasis?

A

Cholesterol supersaturation: Normally, bile can dissolve the amount of cholesterol excreted by the liver. But if the liver produces more cholesterol than bile can dissolve, the excess cholesterol may precipitate as crystals. Crystals are trapped in gallbladder mucus, producing gallbladder sludge. With time, the crystals may grow to form stones and occlude the ducts which ultimately produce the gallstone disease.
Excess bilirubin: Bilirubin, a yellow pigment derived from the breakdown of red blood cells, is secreted into bile by liver cells. Certain hematologic conditions cause the liver to make too much bilirubin through the processing of breakdown of hemoglobin. This excess bilirubin may also cause gallstone formation.
Gallbladder hypomotility or impaired contractility: If the gallbladder does not empty effectively, bile may become concentrated and form gallstones.

23
Q

What is the pathogenesis of pancreatitis?

A

premature activation of pancreatic enzymes which cause pancreatic destruction and activation of inflammatory cascade which can cause hemorrhaging

24
Q

Where can pancreatic cancer metastasize to?

A

metastasizes to the liver

25
Q

what are risk factors of pancreatic cancer?

A

smoking is the top, then tnon o blood type, diabetes, and chronic pancreatitis

26
Q

what are causes of pylric stenosis?

A
  1. deficiency in nitric oxide synthase containing neurons
  2. abnormal innervation of the myenterix plexus
  3. infantile hypergastrinemia
  4. increased gastric secretion by mom in the third trimester
27
Q

what is the difference between physiologic jaundice vs pathological jaundice?

A

Physiologic jaundice develops during the 2ND or 3RD day after birth and subsides in 1 – 2 weeks in full term infants. Caused by mild unconjugated (indirect) hyperbilirubinemia
Pathologic hyperbilirubinemia is the development of increased bilirubin after 4-5 weeks of age, this jaundice is high and persistent

28
Q

what is the hallmark sign of endometrial cancer?

A

postmenopausal bleeding

29
Q

what are risk factors of ovarian cancer?

A
  1. early menarche or late menopause
  2. family history of reproductive cancers
  3. endometriosis
  4. use of fertility drugs
  5. genetic factors (BRCA 1, BRCA2, or Tuner’s syndrome). more commonly associated with BRCA 1
30
Q

what are signs of breast cancer?

A

painless lump, nipple retraction, dimpling of breast tissue, swollen axillary nodes, nipple discharge in non lactating women

31
Q

how can one confirm testicular cancer?

A

through surgery and biopsy

32
Q

what is the sign of testicular cancer?

A

a painless testicular mass, they are slow growing. may have testicular heaviness or dull ache in the lower abdomen.

33
Q

Where does testicular cancer spread to?

A

testis cancer has a very predictable pattern of spread. The first place these cancers typically spread is to the lymph nodes around the kidneys, an area called the retroperitoneum.then the brain, and lungs.

34
Q

what is the genetic risk of prostate cancer?

A

BRCA 2 increases the risk of prostate cancer more than BRCA 1w

35
Q

where does prostate cancer metastasize to?

A

the liver, vertebrae, and pelvic bones

36
Q

what type of diet should those with prosate cancer be on?

A

high fiber diets

37
Q

how does cervical cancer occur?

A

by HPV virus which cause precancerous dysplasia and cervical carcinoma in situ

38
Q

what is the treatment for ascites?

A

Ascites is treated with a low-sodium diet, diuretics, removing the fluid, or surgery to reroute blood flow. Reducing sodium is a first line therapy for ascites.

39
Q

what are clinical manifestations of neprholithiasis?

A

excruciating flank pain that radiates to the groin
anuria and hematuria are also present

40
Q

what is the most common cause of peptic ulcers?

A

h pylori infection

41
Q

how does hypercalicuria occur?

A

Hypercalciuria = intestinal hyperabsorption of dietary calcium

42
Q

what occurs in the prodromal phase of hepatitis?

A

profound anorexia, malaise, nausea and vomiting, a newly developed distaste for cigarettes (in smokers), and often fever or right upper quadrant abdominal pain. hyperalgesia

43
Q

what does benign prostatic hyperplasia lead to?

A

hydronephrosis and increased creatinine

44
Q

how many grams of glucose do the kidneys normally filter?

A

180 grams

45
Q

how does progressive nephron injury effect angiotensin II?

A

it will increase/elevate angiotensin II

46
Q

what medications cause acute tubular necrosis?

A

gentamicin and tobramycin

47
Q

what is the most common clinical manifestation of hypertension induced splenomegaly?

A

thrombocytopenia

48
Q

when does cleft lip occur in the child?

A

The incomplete fusion of the nasomedial and intermaxillary process during THE 4TH WEEK of
gestation causes CLEFT LIP

49
Q

what causes BPH?

A

it is an enlargement of the prostate gland which compresses the urethra where it passes through the prostate resulting in an outlet obstruction

50
Q

what is the treatment for pre renal AKI?

A

isotonic fluids or 0.9 normal saline. the gold standard is to see a downward trend in creatinine