Chapter 10 Flashcards

Question

What does graves disease come from?

Answer 1

secondary hyperthyroidism

Answer 2

Autoimmune disorder of unknown etiology | Thyroid stimulating antibodies (TSAbs)

Answer 3

``` Protrusion of the eyeballs -Prone to corneal ulcerations → blindness -Extraocular muscle paralysis -Involvement of the optic nerve ```

Answer 4

Increased O2 consumption Shortness of breath Hypermetabolism Weight loss w/ large appetite, fatigue, muscle cramps, heat intolerance, excessive sweating Excessive SNS activity Nervousness, irritability, tachycardia, palpitations

Answer 5

Aldosterone (Mineralocorticoid) Cortisol (Glucocorticoid) Androgens (Adrenal sex hormones) Catecholamines (epinephrine, norepinephrine and dopamine

Answer 6

Regulation of Na+, K+ & H2O

Answer 7

``` Glucose metabolism Protein metabolism Fat metabolism Anti-inflammatory Psychic effects Facilitates tissue response to humoral and neural influences ```

Answer 8

Secondary sex characteristics

Answer 9

Aldosterone deficiency Hyponatremia, hyperkalemia, ECF deficits, ↓ CO Orthostatic hypotension, dehydration, weakness & fatigue ``` Glucocorticoid deficiency Poor tolerance of stress Hypoglycemia Lethargy Gastrointestinal symptoms Anorexia, nausea, vomiting & diarrhea ``` ↑ ACTH (adrenalcorticotropic hormone) Hyperpigmentation Exposed and unexposed skin

Answer 10

Insufficient adrenal function to respond to stressors Etiology Minor illness or injury abrupt withdrawal of long term supplemental steroids such as prednisone Pathogenesis Unable to increase the secretion of hormones in response to stress

Answer 11

``` Nausea & vomiting Muscular weakness Severe hypotension Dehydration Vascular collapse ```

Answer 12

Cushing Syndrome” Benign or malignant adrenal tumor “Cushing’s disease” Pituitary tumor → ↑ ACTH Other Long term glucocorticoid therapy “Iatrogenic Cushing’s Syndrome”

Answer 13

Exaggeration of the effects of cortisol Glucose intolerance Altered fat metabolism Buffalo hump, protruding abdomen, moon face Protein breakdown and muscle wasting Osteoporosis Purple striate

Answer 14

Deficiency of or decreased response to ADH Neurologic (brain) Defective synthesis or release of ADH Nephrogenic (kidney) Loss of renal response to ADH

Answer 15

Head trauma | Surgery near the hypothalamic-posterior stalk

Answer 16

Acquired Genetic Lithium, hyperkalemia, hypercalcemia Interfere with the action of ADH in the collecting tubules

Answer 17

``` Polyuria (up to 20 L/day) Polydipsia (abnormal thirst) Hypernatremia Inadequate access to water Hypertonic dehydration and increased serum osmolality ``` * Need synthetic anti-diuretic hormone

Answer 18

too much adh

Answer 19

Brain tumors Hydrocephalus Head injury Can occur with cancer

Answer 20

Decreased serum osmolality Fluid volume excess w/ dilutional hyponatremia (low sodium) Decreased urine output ↓ Hematocrit related to dilution *Need fluid restriction or sodium replacement

Answer 21

causes cells to release stored energy into the blood

Answer 22

allows cells to take up glucose from the blood; the key that opens the door

Answer 23

slows glucose absorption in small intestine; suppresses glucagon secretion

Answer 24

decreases GI activity; suppresses glucagon and insulin secretion

Answer 25

converted to fat for storage

Answer 26

the formation of glycogen from glucose.

Answer 27

when the liver converts amino acids, glycerol and lactic acid into glucose that is stored as glycogen or released directly into the blood stream.

Answer 28

when the liver breaks down stored glycogen via glucagon back to glucose.

Answer 29

< 140 mg/dl

Answer 30

``` 1. Deficiency of insulin secreted by the beta cells of the islets of Langerhans OR 2. Defective insulin receptors OR 3. Early destruction of insulin ```

Answer 31

pancreatic beta cell destruction predominantly by an autoimmune process w/ absolute insulin deficiency

Answer 32

a combination of beta cell dysfunction and insulin resistance

Answer 33

Destruction of Beta cells (90 %) lack of insulin hyperglycemia Glucose cannot get into cells without insulin. Fats and proteins broken down in liver to provide energy to cells. Cells need insulin for glucose to enter cell.

Answer 34

Impaired release of insulin Inadequate or defective insulin receptors Increased hepatic glucose production

Answer 35

Greater risk for developing type 2 diabetes ↑ resistance to the action of insulin impaired suppression of glucose production in the liver Increased circulating free fatty acids (FFA’s)

Answer 36

``` Elevated triglyceride levels Low HDL lipoproteins Hypertension Elevated C-reactive protein (inflammation) Vascular disease Peripheral Cerebral Coronary ```

Answer 37

Glucose intolerance during pregnancy

Answer 38

Family history of DM Heavy for date babies 5 or more pregnancies History of stillbirth or fetal anomalies

Answer 39

: FPG >126mg/dl or OGTT > 140 mg/dl

Answer 40

Hormonal changes of pregnancy changes in metabolism which result in impaired glucose tolerance

Answer 41

Increased risk of maternal and/or fetal demise Increased risk of fetal abnormalities macrosomia, hypoglycemia, polycythemia, hypocalcemia, hyperbilirubinemia

Answer 42

Onset Type 1 rapid Type 2 slow Hyperglycemia (fasting plasma glucose [FPG] > 126 mg/dl) Normal 80-90 mg/dl Polydypsia (excessive or extreme thirst) Polyphagia (excessive or extreme hunger) Much less common in Type 2 Polyuria (excessive or extreme urination) Weight loss except in type 2, Somnolence, Fatigue, Blurred vision

Answer 43

Diabetic ketoacidosis Hyperglycemic hyperosmolar state Hypoglycemia

Answer 44

Macroangiopathy Microangiopathy Neuropathy Nephropathy

Answer 45

- Characterized by hyperglycemia, ketosis and acidosis - Fat & protein breakdown in absence of insulin ketoacidosis (ketones made from this process and pH of blood decreases)

Answer 46

Severe stress (release of counter regulatory hormones) cortisol, epinephrine, glucagon) Infection Non-compliance with insulin injections

Answer 47

``` Hyperglycemia > 250 mg/dl Metabolic acidosis Low serum bicarbonate and Low pH Osmotic diuresis dehydration Electrolyte loss of Sodium and Potassium through urination and vomiting Glucosuria Ketonuria Fruity breath, deep and labored breathing ```

Answer 48

``` Type 2 DM Severe hyperglycemia > 600 mg/dl Hyper serum osmolarity >320 mOsm/L Severe Dehydration with neurologic signs (decreased mental state) Absence of ketoacidosis Potassium depletion from diuresis ```

Answer 49

Increased resistance to insulin, elderly, dehydration

Answer 50

``` Severe dehydration Elevated serum osmolality > 320 mOsm/L Decrease in sensorium → coma Hyperthermia Seizures ```

Answer 51

Relative excess insulin in the blood | Blood glucose below normal (< 50-60 mg/dl)

Answer 52

Headache Vague feeling of abnormal mental state Difficulty with problem solving

Answer 53

Sweating Shaking Palpitations Tachycardia

Answer 54

Thickening of the capillary basement membrane | Chronic Hyperglycemia proliferation of basement membrane cells ↓ tissue perfusion

Answer 55

Pain Paresthesia (numbness & tingling) Loss of sensation Diminished reflexes

Answer 56

leads to nerve cell damage. Loss of sensation increases diabetic foot ulcers because of increased risk of injury.

Answer 57

Microaneurysms in the retinal arterioles hemorrhage scarring blindness

Answer 58

most common cause of end stage renal disease (ESRD) aka kidney failure -Hyperglycemia along with hypertension --> destruction of nephrons

Answer 59

- Peripheral vascular disease and CAD - Hyperglycemia is accumulation of glucose bound end products attach to vessel walls and Lipids deposit (hyperlipidemia)