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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
Glucagon stimulates ____ in liver
glycogenolysis (breakdown of glycogen) and gluconeogenesis -- both increase sugar in the blood
26
Incretins have a _______ effect (GIP and GLP-1)
antihyperglycemic effect -they promote glucose-dependent insulin secretion -inhibit glucagon synthesis -delay gastric emptying
27
What drug works to increase GLP-1?
-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
28
Decreased activity of ______ is associated with insulin resistance
Ghrelin
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Ghrelin. What is it? What does it do? What happens when it's decreased?
-produced by stomach and pancreas -increases appetite -stimulated by fasting -decreased activity of ghrelin is associated with insulin resistance
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Women with ______ have a high risk for metabolic syndrome and are 7 times more likely to development DM
polycystic ovary syndrome
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**What is the criteria for metabolic syndrome?**
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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Pathophysiology of DM What does it begin with?
-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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Adipokines d/t obesity lead to decrease in what and increase in what? Increase in serum fatty acids (SFAs) cause \_\_\_\_\_\_\_\_
- production of insulin and increase in insulin resistance - ***_cause lipotoxicity. This promotes inflammation and apoptosis,_*** as well as decreased tissue response to insulin
34
beta cell dysfunction in T2DM caused by?
- glucotoxicity, lipotoxicity, and inflammatory cytokines - oxidative stress - production of reactive oxygen species (ROS) - autophagy of beta cells
35
in T2DM the aplha cells are less responsive to elevated glucose levels and are not \_\_\_\_\_\_\_
turned off therefore causing more secretion of glucagon
36
Amylin does what and what is the drug that acts like it?
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
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decreased levels of ghrelin are associated with?
hyperinsulinemia and hyperleptinemia \*hyperinsulinemia is d/t increase in insulin resistance d/t decreased ghrelin
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Clinical Manifestations of T2DM
- 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
Diagnostic Criteria for DM
-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
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Diagnostic Criteria for Prediabetes
- 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%
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Target goal for HbA1C w/type II diabetes
less than or equal to 6.5
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First Line Drug for Type2DM
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Hyperosmolar Hyperglycemia Nonketotic Syndrome What causes it? What does it do to glucose levels? What can it result in?
- 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)
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Microvascular disease in Type2DM causes what? Main thing you need to know for exam?
- **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
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Neuropathy in Type 2DM
- 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**)
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Retinopathy Stage I Non-proliferative = ?
thickening of capillary baseement membrane
48
What is the first sign of nephropathy?
Microalbuminuria - all diabetics should be screened for urine microalbumin annually
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Pt w/Type II diabetes experiencing a lot of nausea, bloating, and constipation...what could be causing this?
Could be gastroparesis
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Type 1A DM caused by? Secondary Type3c type 1 DM caused by?
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
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Type 1 DM Effects of Destruction of Pancreatic Cells
- lack of amylin and and insulin from beta cells - relative excess of glucagon - both alpha and beta cells functions are abnormal - causes hyperglycemia
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Clinical Manifestations of Type 1 DM
- 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
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Tx for Type 1 DM
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)
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Remember that with Type 1 you never have a period of high insulin and no insulin resistance
...remember type 2 diabetes you go through a period of having very high insulin levels d/t insulin resistance
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Diabetic Ketoacidosis Causes? What happens in liver? What happens with K+? What happens with fats?
- 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
Because K+ is already low and you give insulin what can happen?
- 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
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Complications for type 1 and type 2 DM are the same
...
60
What are bone changes with DM called?
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
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New vessels (proliferative) in eyes from DM can cause \_\_\_\_\_\_\_
retinopathy
62
Explain the process of thyroid secretion from hypothalamus to thyroid gland
TRH from hypothalamus goes to ant pit and ant pit secretes TSH and THS travels to thyroid and thyroid releases T3 and T4
63
What 4 things can cause hyperthyroidism
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
s/s of hyperthyroidism
-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
what causes ophthalmopathy with Graves disease
- increased secretion of hyaluronic acid, orbital fat accumulation, inflammation, and edema of the orbital contents - can cause diplopia
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s/s of hypothyroid (more of an anabolic state)
- 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
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Myxedema - what causes it and what are the symptoms - what is myxedema coma? - tx for myxedema coma?
- 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
Primary Hypothyroidism Etiologies
- 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
If there is a problem with (low function) antreior pituitary would also see what?
Low TSH, FSH, ACTH, GH, PROLACTIN
71
HIGH TSH AND LOW T4
PRIMARY HYPOTHYROIDISM
72
HIGH TSH AND NORMAL T4
SUBCLINICAL HYPOTHYROIDISM. MOST CASES WILL END UP W/FULL BLOWN HYPOTHYROIDISM. CHECK THYROID ANTIBODY IN THIS PERSON. COULD BE HASHIMOTO'S
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LOW TSH AND HIGH T4
PRIMARY HYPERTHYROIDISM. THIS COULD BE GRAVE'S DISEASE
74
HIGH TSH AND HIGH T4
SECONDARY HYPERTHYRODISM. PIT TSH SEECRETING ADENOMA.
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LOW TSH AND LOW T4
SECONDARY HYPOTHYROIDISM. FAILURE OF PIT GLAND. WILL SEE DECREASE IN OTHER HORMONES.
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ADDISON DISEASE - WHAT IS IT? - WHAT CAUSES IT? - TX?
- 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
Addisonian Crisis
Severe hypotension and vascular collapse -extracellular volume depletion, and some precipitating stressor (infection, v/d/d, decreased vasomotor tone caused by cortisol deficiency)
78
RF is what type of antibody What is a more specific serum marker for RA?
IgM-type autoantibodies specific: ACPA - anticitrullinated protein antibody - can be present for decades before synovial changes are present
79
what happens in hyperaldosteronism? what causes it? s/s?
- 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
Manifestation of pancreatitis - caused by? Pancreatitis in severe cases can lead to? Clinical findings? Labs?
- 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
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Patho Exam 2 (4 decks)

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