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Patho Exam 2 > Endocrine > Flashcards

Endocrine Flashcards

1
Q

Functions of the pancreas _____ and ______

A

exocrine and endocrine -exocrine think GI enzymes -endocrine: release directly into bloodstream and move to target organ

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2
Q

Islet of Langerhans and function of each of the cells

A

part of the pancreas with alpha and beta cells beta cells make insulin and amylin alpha cells make glucagon

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3
Q

Alpha and beta cells communicate using

A

paracrine function

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4
Q

Brain needs constant supply of? But brain does not need what to use it?

A

Glucose, and the brain does not need insulin to use it

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5
Q

What are some different ways that beta cells are stimulated to produce insulin?

A

-parasympathetic NS stimulation -gastric production of incretins (GIP, GLP-1) -high glucose, amino acids, fats in BLOOD

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6
Q

What are incretins? Where are they produced? What are the main ones here?

A

Incretins are a group of metabolic hormones that stimulate a decrease in blood glucose levels. Incretins are released after eating and augment the secretion of insulin released from pancreatic beta cells of the islets of Langerhans by a blood glucose-dependent mechanism. Incretins are GIP, GLP-1 and are produced by GI

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7
Q

Actions of insulin

A

Liver - glucose uptake, glyconeogenesis (formation of glucose), fatty acid synthesis Fat - lipogenesis (generation of more fat cells) and fat storage Muscle cells - glucose and K+ into cell (glycogen formation)

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8
Q

Amylin, where is it produced and what is it?

A

Produced by beta cells in pancreas = satiety and feeling of fullness; also delays nutrient uptake so not such a high rise in blood sugar Also shuts off glucagon production

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9
Q

Insulin secretion by beta cells is inhibited by?

A

low glucose, high insulin, sympathetic NS stimulation, PG

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10
Q

What does insulin do? Which cells do not need insulin?

A

-Allows glucose and K+ into cells -Drives Na/K pump -Brain, RBCs, kidneys

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11
Q

Alpha cells are stimulated to produce glucagon when…

A

-hypoglycemia -prolonged fasting -exercise -protein rich meals -SNS activation -amino acids

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12
Q

Actions of glucagon

A

-liver: glycogenolysis, gluconeogenesis -fat tissue: lipolysis, ketogenesis -kidney: gluconeogenesis

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13
Q

What causes alpha cell inhibition to stop glucagon release

A

-high glucose in blood -beta cells (when glucose is high) -GLP-1 (remember this is an incretin produced by GI) these incretins work to increase insulin production by beta cells

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14
Q

Is insulin anabolic or catabolic?

A

Anabolic - promotes synthesis and storage of protein, CHO, and fat

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15
Q

Where does insulin mainly function? where is it not needed?

A

liver, muscle cells, adipose tissue not needed in brain, RBCs, lens of the eye, and kidney

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16
Q

what stimulates insulin secretion

A

-elevated glucose -elevated amino acids -gastric secretions -PSNS activation

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17
Q

what inhibits insulin secretion

A

-low blood glucose -high insulin levels (negative feedback) -SNS activation

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18
Q

function of glucagon

A

stimulates liver to produce glucose

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19
Q

glucagon is released in response to

A

low glucose levels and high protein meal

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20
Q

function of amylin

A

-antihyperglycemic effect -secreted by beta cells -slows nutrient uptake -suppresses glucagon secretion -promotes satiety -DRUGS CALLED AMYLOMIMETICS are used in management of both type 1 and type 2 diabetes (Pramlintide)

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21
Q

Incretins GIP and GLP-1 do what? What do GIP and GLP-1 stand for

A

stimulate beta cells to produce insulin and amylin, inhibits alpha cell function Glucose-dependent insulinotropic peptide (GIP) Glucagon-like peptide (GLP-1)

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22
Q

How is insulin anabolic?

A

stimulates synthesis of protein, CHO, lipids and nucleic acids *keep in mind that since it does stimulate synthesis of lipids, an increase in insulin does make people gain weight

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23
Q

if you give someone insulin remember that it can cause _____

A

hypokalemia this is because insulin increases the uptake of both glucose and K by cells

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24
Q

Remember that insulin is secreted in response to _______. And remember that _______ action is ________

A

glucagon secretion glucagon is an INSULIN ANTAGONIST

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25
Q

Glucagon stimulates ____ in liver

A

glycogenolysis (breakdown of glycogen) and gluconeogenesis – both increase sugar in the blood

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26
Q

Incretins have a _______ effect (GIP and GLP-1)

A

antihyperglycemic effect -they promote glucose-dependent insulin secretion -inhibit glucagon synthesis -delay gastric emptying

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27
Q

What drug works to increase GLP-1?

A

-GLP-1 is metabolized in the body by the enzyme DDP IV -Drugs that inhibit DDP IV are called GLIPTINS and are used in management of T2DM

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28
Q

Decreased activity of ______ is associated with insulin resistance

A

Ghrelin

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29
Q

Ghrelin. What is it? What does it do? What happens when it’s decreased?

A

-produced by stomach and pancreas -increases appetite -stimulated by fasting -decreased activity of ghrelin is associated with insulin resistance

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30
Q

Women with ______ have a high risk for metabolic syndrome and are 7 times more likely to development DM

A

polycystic ovary syndrome

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31
Q

What is the criteria for metabolic syndrome?

A

Must have 3/5

  • increased waist circumference (>40 inches in men; >35 in women)
  • Plasma triglycerides > or equal to 150mg/dL (normal triglyceride level is below 150)
  • plasma HDL cholesterol <40mg/dL in men and <50 mg/dL in women
  • blood pressure > or equal to 130/85mmHg
  • fasting plasma glucose > or equal to 100mg/dL
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32
Q

Pathophysiology of DM

What does it begin with?

A

-It does not start with high blood glucose, it starts with increased insulin resistance and increased insulin levels. May be present for years before high blood sugar.

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33
Q

Adipokines d/t obesity lead to decrease in what and increase in what? Increase in serum fatty acids (SFAs) cause ________

A
  • production of insulin and increase in insulin resistance
  • cause lipotoxicity. This promotes inflammation and apoptosis, as well as decreased tissue response to insulin
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34
Q

beta cell dysfunction in T2DM caused by?

A
  • glucotoxicity, lipotoxicity, and inflammatory cytokines
  • oxidative stress
  • production of reactive oxygen species (ROS)
  • autophagy of beta cells
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35
Q

in T2DM the aplha cells are less responsive to elevated glucose levels and are not _______

A

turned off therefore causing more secretion of glucagon

36
Q

Amylin does what and what is the drug that acts like it?

A

amylin delays gastric emptying, increases satiety, and suppresses glucagon release

-pramlintide, a synthetic analog of amylin, is used for tx in type 1 and type 2 DM. Really this is the ONLY oral drug approved for type 1 diabetes.

*Remember that amylin is also released by beta cells

37
Q

decreased levels of ghrelin are associated with?

A

hyperinsulinemia and hyperleptinemia

*hyperinsulinemia is d/t increase in insulin resistance d/t decreased ghrelin

38
Q

Clinical Manifestations of T2DM

A
  • pruritis d/t dry skin
  • frequent infections d/t oxidative stress on immune cells
  • fatigue
  • metabolic syndrome
  • visual changes (fluctuations in fluid levels in the eyes)
  • neuropathy
  • Late: CAD, PAD, CVD, retinopathy, nephropathy
39
Q

Diagnostic Criteria for DM

A

-A1C > or equal to 6.5

OR

FPG > or equal to 126; remember fasting is defined as no caloric intake for at least 8 hours

OR

2-hr plasma glucose > or equal to 200mg/dL during an OGTT

OR

In a patient with classic symptoms of hyperglycemia or hyperglycemic crisis, a random plasma glucose of greater than or equal to 200mg/dL

40
Q

Diagnostic Criteria for Prediabetes

A
  • FPG of 100-126 mg/dL
  • 2-hr PG in the range of 140 to 199 mg/dL during OGTT
  • HbA1c 5.7 to 6.4%
41
Q

Target goal for HbA1C w/type II diabetes

A

less than or equal to 6.5

42
Q

First Line Drug for Type2DM

A
43
Q

Hyperosmolar Hyperglycemia Nonketotic Syndrome

What causes it?

What does it do to glucose levels?

What can it result in?

A
  • precipitated by infection, medications (like steroids), or non-adherence
  • more common in type 2DM
  • very high glucose levels (highere than DKA)
  • severe volume dificiency d/t glucosuria
  • no ketosis takes place
  • intracellular dehydration, increased serum osmolality
  • stupor and coma (CNS depression)
44
Q
A
45
Q

Microvascular disease in Type2DM causes what? Main thing you need to know for exam?

A
  • thickening of capillary basement membrane (she said this was on the exam)
  • vascular cell proliferation, angiogenesis (formation of new vessels)
  • lots of inflammatory processes occurring (ROS, lipid oxidation, inactivation of NO, etc.)
  • hyperplasia of endothelial cells
  • thrombosis
  • decreased tissue perfusion
  • tissue hypoxia and ischemia
  • retinopathy, nephropathy, neuropathy
46
Q

Neuropathy in Type 2DM

A
  • neuropathic pain, loss of sensation (foot ulcers)
  • sensory loss of proprioception and vibration (falls). s/s of this could be dizziness
  • Autonomic neuropathy: GI problems like gastroparesis, loss of bladder & sex function, sweating and body temperature regulation problems, cardiovascualr autonomic neuropathy (painless MI)
47
Q

Retinopathy Stage I Non-proliferative = ?

A

thickening of capillary baseement membrane

48
Q

What is the first sign of nephropathy?

A

Microalbuminuria - all diabetics should be screened for urine microalbumin annually

49
Q

Pt w/Type II diabetes experiencing a lot of nausea, bloating, and constipation…what could be causing this?

A

Could be gastroparesis

50
Q
A
51
Q

Type 1A DM caused by?

Secondary Type3c type 1 DM caused by?

A

Type IV hypersensitivity rxn - autoimmune process that causes destruction of beta cells by autoantibodies, T-cells, and macrophages

Secondary caused by chronic pancreatitis causing autodigestion of beta cells

52
Q

Type 1 DM Effects of Destruction of Pancreatic Cells

A
  • lack of amylin and and insulin from beta cells
  • relative excess of glucagon
  • both alpha and beta cells functions are abnormal
  • causes hyperglycemia
53
Q

Clinical Manifestations of Type 1 DM

A
  • 80-90% loss of function of beta cells before hyperglycemia develops (latent period)
  • polydipsia, polyuria, polyphagia, weight loss, and fatigue
  • wt loss d/t STARVING cells and muscles
54
Q

Tx for Type 1 DM

A

Insulin, meal planning, exercise, monitoring blood glucose

Transplant: Islet cells and the whole pancreas

Amylin synthetic drug that delays gastric emptying, supprsses glucagon, and increases satiety (Pramlintide)

55
Q

Remember that with Type 1 you never have a period of high insulin and no insulin resistance

A

…remember type 2 diabetes you go through a period of having very high insulin levels d/t insulin resistance

56
Q
A
57
Q

Diabetic Ketoacidosis

Causes?

What happens in liver?

What happens with K+?

What happens with fats?

A
  • precipitated by illness, stress, or failure to take insulin
  • liver: gluconeogenesis (amino acid), glyconeogenesis (CHO) causes increase in blood glucose
  • adipose tissue: lipolysis causes ketone production (fruity breath) which causes acidosis and Kussmaul respirations
  • K+: b/c glucose not able to get into cells you have breakdown of Na/K pump – active transport breaks down. K+ leaves cell by diffusion and gets excreted by urine. So body gets depleted of K+.
  • other s/s: polydipsia, polyuria, dehydration, and wt loss
58
Q

Because K+ is already low and you give insulin what can happen?

A
  • insulin causes K+ to go back into cell and this can cause hypokalemia
  • give insulin with K+ if patient has ketoacidosis to avoid heart problems
59
Q

Complications for type 1 and type 2 DM are the same

A

…

60
Q

What are bone changes with DM called?

A

Charcot foot

Charcot foot is a condition causing weakening of the bones in the foot that can occur in people who have significant nerve damage

61
Q

New vessels (proliferative) in eyes from DM can cause _______

A

retinopathy

62
Q

Explain the process of thyroid secretion from hypothalamus to thyroid gland

A

TRH from hypothalamus goes to ant pit and ant pit secretes TSH and THS travels to thyroid and thyroid releases T3 and T4

63
Q

What 4 things can cause hyperthyroidism

A

1- Grave’s disease (Type 2 Hypersensitivity) - antibodies against receptor bind TSH receptor and cause overproduction of thyroid hormone. TSh will be low, but doesn’t make a difference b/c antibodies act like TSH

2- toxic multinodular goiter

3- follicular adenoma

4- thyroid medication (iatrogenic - illness relating to medical tx)

These are all primary thyroid problems

64
Q

s/s of hyperthyroidism

A

-fatigue, wt loss, insomnia

-thin hair, palmar erythema, sweating, pretibial myexedma

-anxiety

-exophthalmos

  • increased CO, resting tachycardia, SVT
  • dyspnea, reduced vital capacity
  • n/v, loose stools, anorexia, abd pain
  • olingomenorrhea or amenorrhea ED, decreased libido
  • HYPERCALCEMIA d/t increased bone resorption causes, osteoporosis, decreased sensitivity to insulin
  • increased metabolism, decreased tissue stores of vitamins and nutrients, decreased lipid levels
65
Q

what causes ophthalmopathy with Graves disease

A
  • increased secretion of hyaluronic acid, orbital fat accumulation, inflammation, and edema of the orbital contents
  • can cause diplopia
66
Q

s/s of hypothyroid (more of an anabolic state)

A
  • dry skin, brittle hair, COOL skin
  • fatigue, weight gain, decreased appetite
  • dyspnea, hypoventilation, CO2 retention from not breathing as well
  • decreased SV, decreased HR, HTN, hypertrophy - enlarged heart
  • elevated lipids
  • constipation
  • menorrhagia, decreased libido
  • decreased DTRs
  • increase in prolactin, decrease in bone density
  • decreased GFR, reduced water excretion = water retention, dilutional hyponatremia, decreased erythropoietin
67
Q
A
68
Q

Myxedema - what causes it and what are the symptoms

  • what is myxedema coma?
  • tx for myxedema coma?
A
  • hypothyroidism causes it
  • nonpitting, boggy edema, especially around the eyes, hands, and feet; thickening of the tongue
  • coma: medical emergency, diminished LOC, hypothermia w/o shivering, hypoventilation, hypotension, hypoglycemia (think increased insulin sensitivity), lactic acidosis, coma, hyponatremia

tx for myxedema coma: thyroid hormone combined w/circulatory and ventilatory support; management of hyponatremia and hypothermia

69
Q

Primary Hypothyroidism Etiologies

A
  • Iodine deficiency (most common cause worldwide)
  • Most common etiology in US is Hashimoto disease - autoimmune thyroiditis. Type IV hypersensitivity reaction (T-cell mediated). Autoreactive T lymphocytes destroy thyroid tissue
  • Iatrogenic hypothyroidism - surgery, radiation, medications (lithium, amiodarone)
70
Q

If there is a problem with (low function) antreior pituitary would also see what?

A

Low TSH, FSH, ACTH, GH, PROLACTIN

71
Q

HIGH TSH AND LOW T4

A

PRIMARY HYPOTHYROIDISM

72
Q

HIGH TSH AND NORMAL T4

A

SUBCLINICAL HYPOTHYROIDISM. MOST CASES WILL END UP W/FULL BLOWN HYPOTHYROIDISM. CHECK THYROID ANTIBODY IN THIS PERSON. COULD BE HASHIMOTO’S

73
Q

LOW TSH AND HIGH T4

A

PRIMARY HYPERTHYROIDISM. THIS COULD BE GRAVE’S DISEASE

74
Q

HIGH TSH AND HIGH T4

A

SECONDARY HYPERTHYRODISM. PIT TSH SEECRETING ADENOMA.

75
Q

LOW TSH AND LOW T4

A

SECONDARY HYPOTHYROIDISM. FAILURE OF PIT GLAND. WILL SEE DECREASE IN OTHER HORMONES.

76
Q

ADDISON DISEASE

  • WHAT IS IT?
  • WHAT CAUSES IT?
  • TX?
A
  • ADDISON DISEASE IS LOW CORTISOL AND LOW ALDOSTERONE. ACTH will be high beecause attempt at adrenal gland to secrete more
  • s/s include fatigue, electrolyte imbalances, vitiligo, weakness and easy fatigability that worsens as day progresses. Hypoglycemia, hypotension, decreased metabolism of proteins. Problems with RAAS
  • absence of cortisol leads to decreased glucogenesis, decreased glycogen storage by liver, decreased metabolism of proteins, increased insulin sensitivity
  • 50-70% of individuals have autoantibodies agnd autoreactive T cells specific to adrenal cortical cells. The most common cause of Addison disease in US is autoimmune destruction of the adrenal cortex and it is more common in women
77
Q

Addisonian Crisis

A

Severe hypotension and vascular collapse

-extracellular volume depletion, and some precipitating stressor (infection, v/d/d, decreased vasomotor tone caused by cortisol deficiency)

78
Q

RF is what type of antibody

What is a more specific serum marker for RA?

A

IgM-type autoantibodies

specific: ACPA - anticitrullinated protein antibody - can be present for decades before synovial changes are present

79
Q

what happens in hyperaldosteronism? what causes it? s/s?

A
  • increase in Na+ and water retention, decrease K+
  • causes increase in blood pressure
  • Causes: idiopathic, CONN SYNDROME: adenoma or tumor secretes too much aldosterone from adrenal gland, familial hyperaldosteronism
  • Secondary cause is excess renin secretion from kidney
  • hyperaldosteronism leads to hypernatremia, hypokalemia, loss of H+ ions and metabolic alkalosis
  • s/s: h/a, facial flushing, HTN; s/s r/t hypokalemia include constipation, weakness, and changes in heart rhythm
80
Q

Manifestation of pancreatitis - caused by?

Pancreatitis in severe cases can lead to?

Clinical findings? Labs?

A
  • epigastric pain that radiates to BACK
  • caused by autodigestion of exocrine cells (acinar cells w/i pancreas)
  • pancreatitis can lead to sepsis and multiple organ system failure, ARDS, etc.
  • Elevated lipase is PRIMARY dx marker; elevated amylase is not specific; elevation of trypsin, CRP and BUN
  • results in weight loss, steatorrhea, diabetes
81
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Patho Exam 2 (4 decks)

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