Patho Final

Front 1

How are hormones carried?

Back 1

-body fluids
-peptide and protein hormones are water soluble=travel freely in blood
-steroid and thyroid hormones need carrier protein to travel in blood

Front 2

Target organ

Back 2

-can act on organ far away, locally (paracrine)
-or the cell it was released from (autocrine)

Front 3

function of the pituitary gland?

Back 3

“Master gland” controls body growth/metabolism, func. of thyroid, glucocorticoid hormone levels, func. of gonads, breast growth/milk production;

Front 4

What hormones are released by pituitary?

Back 4

POSTERIOR: ADH, oxytocin;
ANTERIOR: GH, ACTH, TSH, FSH, LH, prolactin

Front 5

• ADH

Back 5

Increase kidney reabsorption of H2O

Front 6

Oxytocin

Back 6

stim contraction of prego uterus, milk ejection from breast after birth

Front 7

GH

Back 7

somatotropin
-doesn't affect bone itself
stim liver to make IGFs → bone growth @ epiphyseal plate
cartilage growth
stim visceral/endocrine organs
skeletal/cardiac musc, skin, connective tissue growth
pomote protein synth/fat metab,
decrease carb metab;

Front 8

ACTH

Back 8

stim synth/secretion of adrenal cortical horms

Front 9

FSH

Back 9

stim growth of ovarian follicl, ovulation, sperm production

Front 10

LH

Back 10

stim dev of corpus luteum, release oocty, production of estrogen/progesterone

Front 11

Adult excess GH

Back 11

kyphosis, arthraglias, arthritis of spine/hips/knees, all organs increase in size, heart enlargement=accelerated atherosclerosis
GH-induced insulin resistance

Front 12

Adrenal cortex horomones:

Back 12

-minerlacorticoids (aldosterone : conservation of sodium, secretion of potassium, increased water retention, and increased blood pressure),
-glucotcorticoids (cortisole: increase blood sugar through gluconeogenesis;)
androgen sex hormones

Front 13

Adrenal excess:

Back 13

Cushing syndrome: protein breakdown/musc
; osteoporosis; poor glucose metabolism; increase Na retention and K loss
c inhibition of inflammatory/immune response
increase androgen levels (hirsutism, acne, menstrual irreg)

Front 14

• Adrenal insuff mineralcortocoid:

Back 14

increase urinary loss of Na, Cl, H2O,
, decrease cardiac outpur,

Front 15

Adrenal insuff glucocorticoid

Back 15

hypoglycemia, lethargy, weakness, fever, GI Sx-anorexia, nausea, vomiting, wt loss

Front 16

• Cushing

Back 16

hypercortisolism aka excess glucocorticoid production; caused by excessive production of ACTH b/c pituitary tumor, adrenal tumor, or non-pituitary ACTH-secreting tumor

Front 17

• Type I Diabetes

Back 17

beta cell destruction and an absolute insulin deficiency;
autoimmun

Front 18

• Type II Diabetes

Back 18

insulin resistance and relative insulin deficiency
metabolic abnormalities causes
adrenal causes

Front 19

• Gestational Diabetes

Back 19

; pregnancy hormones block insulin from doing its job

Front 20

• Oral glucose tolerance test

Back 20

measures body ability to remove glucose from glood (indicates able to store it). Give pt 75 g conc glucose at 1-2 hr intervals and measure blood glucose, should return to normal 2-3 hrs after ingestion of a glucose load

Front 21

• Glycosylated hemoglobin

Back 21

hbg doesn’t have any glucose when first released from bone marrow, glycosylation is irreversible so level of glucose in hbg shows blood glucose levels over past 6-12 wks (life of RBC)

Front 22

• Diabetic Ketoacidosis

Back 22

Primarily affect Type I
lack of insulin→breakdown of energy stores in fat/muscle→increased amino acids to liver for conversion to glucose and fatty acids for conversion to ketones→high ketone levels→high ketone levels need buffering by bicarb ions→decrease serum bicarb w/increased serum ketones

Front 23

• Hypoglycemia
Two areas of symptoms

Back 23

excess of insulin in blood, below normal blood glucose levels;
rapid onset
1. caused by cerebral func- headache, difficulty problem solving, disturbed/altered behavior, coma, seizure,
2. related to activation of autonomic NS- first parasymp NS cause hunger, then symp NS activated causing anxiety, tachycardia, sweating constriction of skin vessels

Front 24

Treatment of Hypoglycemia

Back 24

treat first w/ 15-20g of concentrated glucose, then give complex carbs once rxn is under control; do not over treat and cause hyperglycemia

Front 25

• Diabetic nephropathy:

Back 25

-increased urinary albumin excretion
-lesions on glomeruli
-impaired blood flow causes progressive loss of renal function until renal failure

Front 26

How does insulin lower blood glucose?

Back 26

-glucose storage as glycogen
-. Prevents fat and glycogen breakdown into glucose,
-Inhibits gluconeogenesis and increases protein synthesis

Front 27

How does insulin act on the body?

Back 27

-Promotes fat storage by increase transport of glucose into fat cells
-Facilitates triglyceride synth from glucose in fat cells, inhibits intracellular breakdown of stored triglycerides
-Increases active transport of amino acids into body cells thus increaseing protein synthesis, inhibits gluconeogenesis

Front 28

amines/amino acids

Back 28

norepinephrine, epinephrine, thyroid hormones

Front 29

peptides/polypeptides/proteins/glycoproteins

Back 29

TRH (thyrotropin releasing hormone), GH, FSH

Front 30

cholesterol derivatives

Back 30

-lipids
-steroids

Front 31

fatty acid derivatives

Back 31

-eicosanoids
-prostaglandins, leukotrienes, thromboxanes

Front 32

Negative affect of exercise with diabetes

Back 32

-risk of hypoglycemia b/c muscles will now increase injected insulin absorption but can’t counterregulate to maintain blood glucose
-in type I can cause higher levels of glucose and ketones in blood while still insulin deficient
-hyperglycemia, ketosis, cardiovascular ischemia and arrhythmias, exacerbation of proliferative retinopathy, lower extremity injury

Front 33

Diabetic retinopathy

Back 33

abnorm retinal vascular permeability

Front 34

Insulin lowers blood glucose by

Back 34

1. Promotes glucose uptake by target cells and provides for glucose storage as glycogen. Promotes fat storage
2. Prevents fat and glycogen breakdown into glucose
3. Inhibits gluconeogenesis and increases protein synthesis

Front 35

in thin descending loop of Henle

Back 35

H2O REABSORBED

Front 36

in thick ascending loop of Henle

Back 36

-Na, Cl, K, Ca, HCO3, Mg REABSORBED
-H SECRETED

Front 37

in early distal tubule

Back 37

Na, Cl, Ca, Mg REABSORBED

Front 38

in late distal tubule/collecting duct principal cells

Back 38

Na, Cl REABSORBED
K SECRETED; ADH-mediated H2O REABSORPTION

Front 39

intercalated cells

Back 39

cells: HCO3, K reabsorbed; H secreted

Front 40

GFR

Back 40

125ml filtrate/min, 1 ml of which is secreted

Front 41

buffers in urine that combine w/ H

Back 41

bicarbonate,
phosphate (HPO4),
ammonia (NH3)

Front 42

vit D activation

Back 42

-occurs in kidney
-activated vit D increases calcium absorption from GI tract,
-helps regulate Ca deposition in bone

Front 43

Etiology of Polycystic Kidney Disease

Back 43

-Defect in the cilia of the epithelial cells
-interfere with fluid absorption or cellular maturation, resulting in cyst formation.
-Mutations in polycystin gene (mediates cell proliferation, differentiation & apoptosis directly)
-Mutations in fibrocystin (regulates cell proliferation & adhesion)

Front 44

Signs & Symptoms of Polycystic Kidney Disease

Back 44

Hypertension

Front 45

Nephrotic Syndrome
S/Sx

Back 45

-↑ glomerular permeability
-Proteinuria: EXCESS protein
-Hypoalbuminemia (With loss of albumin, edema develops because of lack of amino acids for plasma protein synthesis)
-Lipiduria: PRESENCE of lipid in the urine. Compensation: Hyperlipidemia: abnormally elevated levels of triglycerides & LDLs in the blood (atherosclerosis)

Front 46

Minimal-Change Disease

Back 46

0. Diffuse loss of foot processes of cells

Front 47

Membranous Glomerulonephritis

Back 47

thickening of the glomerular basement membrane because of deposits of immune complexes

Front 48

Focal Segmental Glomerulosclerosis

Back 48

Another type of nephrotic syndrome

Front 49

Diabetic Nephropathy (define & etiology)

Back 49

-lesions that occur concurrently in the diabetic kidney
-Caused by:
↑ BP
Microalbumuria (hypoalbumuria)
Poor glycemic control
Smoking
Hyperlipidemia

Front 50

Diabetic Nephropathy s/sx

Back 50

-Kidney Enlargement, Nephron Hypertrophy, Hyperfiltration (Thickening of capillary basement membrane)
-glomerular sclerosis

Front 51

Diabetic Nephropathy . Pathophysiology

Back 51

-↑ work by the kidneys to reabsorb excessive amounts of glucose (hyperfiltration)
-↑ urinary albumin excretion

Front 52

Pyelonephritis
S/Sx

Back 52

-Bacterial infection of the upper urinary tract
-Lower UTI, obstruction of bladder outflow
-polyuria, chills, fever, malaise
-Papillary Necrosis – ischemia of the renal pyramids, renal failure

Front 53

Wilm’s Tumor

Back 53

-malignant embryonic kidney tumor
-Abdominal hypertension
Abdominal pain and/or vomiting
Aniridia – absence of the iris
Hemihypertrophy – enlargement of one side of the face or body
-Sharply demarcated & variably encapsulated

Front 54

Renal Cell Carcinoma
Causes
Symptoms mean
Where located

Back 54

-Heavy smoking, obesity, cystic kidney disease, occupational exposure
-Symptoms mean advanced disease
-PREDOMINANTLY in the cortex

Front 55

Chronic Kidney Disease
-caused by

Back 55

-Permanent loss of nephrons, decline in kidney function leads to failure.
-Stages classified by GFR
- Diabetes
. Hypertension
. Glomerulonephritis
. Lupus
. Polycystic Kidney Disease

Front 56

Chronic Kidney Disease s/sx

Back 56

0. Uremia
. Proteinuria
. Anemia
. Altered fluid & electrolyte ∴ acid imbalance
. Impaired mineral & drug metabolism
. Compensation: Nephrons undergo structural & functional hypertrophy

Front 57

Pathophysiology of Chronic Kidney Disease

Back 57

-Insufficient reabsorption of HCO3- ∴ ↑H+ = Metabolic Acidosis
-Compensation: Bone resorption as a buffer
-Impaired phosphate elimination
. ↑ phosphate = ↓ Ca2+
-Impaired activation of vitamin D
-Anemia, hemolysis: Kidneys are the primary site for erythropoietin
-Associated hypertension (EARLY manifestation of CKD)
.↑ Vascular Volume & resistance

Front 58

Calcium Stones

Back 58

calcium oxalate OR calcium phosphate OR a combination
. Immobility, bone disease, hyperparathyroidism & renal tubular acidosis
. Excessive bone resorption

Front 59

. Magnesium Ammonium Phosphate Stones

Back 59

“struvite stones” or “staghorn stones”
alkaline urine AND in the present of bacteria that contain the enzyme urease
. Urease – splits the urea into ammonia & CO2
. Ammonia (neutral) absorbs H+ ions to so that it becomes more alkaline as an ion
. Alkaline environment ↑ phosphate levels which bind with magnesium to form stones

Front 60

Urinary Retention Congenital Obstructions

Back 60

Girls: Inside the external urinary meatus
Boys: External meatal stenosis
BOTH: spina bifida (herniation)

Front 61

. Acquired Lower Urinary Obstruction & Stasis

Back 61

Girls
. Impaired relaxation of the pelvis
Boys
. External compression of the urethra caused by enlargement of the prostate gland
. Both
. Gonorrhea & STIs
. Bladder tumors

Front 62

Treatment Chronic Kidney Disease

Back 62

Prevention or slow the rate of nephron destruction
Treat UTIs
Treat diabetes, prevent microalbuminuria
Control BP
. Restriction on dietary proteins
. ↓ nitrogenous wastes & ↓ BUN ∴ reduces symptoms
. Avoid protein breakdown for energy
-K restrictions

Front 63

Co-morbid juvenile diabetes

Back 63

. Graves Disease
. Rheumatoid Arthritis
. Addison Disease
. Thyroiditis
. Hypothyroidism

Front 64

Treat Congenital Hypothyroidism

Back 64

hormone replacement. It is important to normalize T4 levels as quickly as possible to minimize developmental issues (i.e. mental retardation)

Front 65

Cause of brittle bone disease

Back 65

-by deficiencies in the synthesis of type I collagen.
-hereditary

Front 66

Treat osteoporosis

Back 66

bisphosphonates (effective inhibitors of bone resorption)
selective estrogen receptor modulators
calcitonin
recombinant parathyroid hormone

Front 67

Rheumatoid Arthritis

Back 67

autoimmune
joint involvement usually is symmetric and polyarticular
fibrosis
“spongy” feeling of joints
neutrophils and macrophages phagocytize the immune complexes and, in the process, release lysosomal enzymes capable of causing destructive changes in the joint cartilage. The inflammatory response that follows attracts additional inflammatory cells
-Pannus

Front 68

Osteoarthritis

Back 68

Breakdown/erosion of synovial joint cartilage resulting in thickening of exposed bone
joint pain – usually worsened by activity and relieved by rest
as “gelling,” involves difficulty initiating joint movement after inactivity
from new bone formation making the joint feel hard

Front 69

Lupus

Back 69

-chronic inflam-matory disease
-rheumatic disease
-formation of autoantibodies and immune complexes (type III hypersensitivity)
-defective elimination of self-reactive B cells with a resultant increase in production of antibodies