Patho Final

STRUCTURE OF ENDOCRINE SYSTEM

1. Glands: pituitary, thyroid, parathyroid, adrenal, pancreas, ovaries, testes
2. Hormones: chemical substances, affect only target cells with receptors - initiate specific functions or activities

HORMONAL REGULATION

1. negative feedback: high levels of a substance inhibit hormone synthesis/secretion. low levels stimulate "THERMOSTAT"
2. positive feedback: high levels stimulate synthesis and secretion, low levels inhibit
3. nervous system: causes release of hormones
4

MECHANISMS OF HORMONAL ALTERATIONS

1. failed feedback systems
2. gland synthesize or release too much
3. gland unable to produce enough
4. hormone degraded or inactivated before reaching target cell
5. target cells do not respond

POSTERIOR PITUITARY FUNCTION

1. antidiuretic hormone (ADH)= fluid balance and water retention.
2. oxytocin= contracts uteres

SYNDROME OF INAPPROPRIATE ADH DEFINITION

high levels ADH: caused by tumors, transient after surgery, meds, infections

PATHO OF SYNDROME OF INAPPROPRIATE ADH

ADH released = H2O retention -> excess fluid volume + dilutional hyponatremia. Renin suppressed causing dec in aldosterone (does not retain Na) and dec reabsorption of Na. Net effect - hyponatremia, hypoosmolarity, water retention

CLINICAL MANIFESTATIONS OF SYNDROME OF INAPPROPRIATE ADH

a. muscle weakness
b. abdominal cramps
c. fatigue
d. headache
e. confusion
f. seizures

DIAGNOSTICS OF SYNDROME OF INAPPROPRIATE ADH

a. serum osmolarity= LOW
b. urine osmolarity= HIGH
c. serum Na=LOW
d. urine output=LOW

TREATMENT OF SYNDROME OF INAPPROPRIATE ADH

a. water restrictions
b. hypertonic saline solution
c. chronic SIADH - meds to inihibit ADH

DIABETES INSIPIDUS DEFINITION

Insufficient ADH or dec action.
Types.
a. neurogenic
b. nephrogenic
c. psychogenic

PATHO DIABETES INSIPIDUS

a. neurogenic - dec in ADH leads to excretion of large amount dilute urine (dehydration & shock)
b. nephrogenic - ADH OK but collecting ducts don't respond

CLINICAL DIABETES INSIPIDUS

a. polyuria (frequent urination)
b. nocturia (night urination)
c. inc thirst
d. fatigue

DIAGNOSTIC TEST OF DIABETES INSIPIDUS

a. serum osmolarity (increase)
b. urine osmolarity (low=dilute)
c. water deprivation study

TREATMENT OF DIABETES INSIPIDUS

a. fluids
b. synthetic ADH
c. meds to enhance ADH

ANTERIOR PITUITARY FUNCTION

1. growth hormone (GH)
2. thyroid stimulating hormone (TSH)
3. adrenocorticotropic hormone (ACTH)
4. prolactin (PR)
5. gonadotropic hormones (FSH, LH)

HYPOPITUITARISM DEFINITION

absence of one hormone to complete failure of all

HYPOPITUITARISM PATHO

infarctions (lack of blood flow) -> tissue necrosis and edema. Tumors -> destruction of gland

HYPOPITUITARISM CLINICAL GENERAL

a. weakness
b. HA
c. sexual dysfunction
d. dec tolerance to stress
e. vision changes

HYPOPITUITARISM CLINICAL PANHYPOPITUITARY

ALL HORMONES ARE ABSENT:
a. cortisol deficiency
b. thyroid deficiency
c. diabetes isipidus
d. gonadal failure
e. dec in GH

DIAGNOSTIC HYPOPITUITARISM

RADIOIMMNOASSAY

TREATMENT OF HYPOPITUITARISM

HORMONE REPLACEMENT

FUNCTION OF PARATHYROID GLAND

Secrete parathyroid hormone (PTH) - regulates calcium level

HYPERPARATHYROIDISM

Excess PTH= Ca levels are increased

PATHO OF HYPERPARATHYROIDISM

a. primary: tumor
b. secondary: response to chronically low Ca levels (renal patients)
c. tertiary: hyperplasia of gland, loss of sensitivity to Ca

HYPERPARATHYROIDISM CLINICAL

a .fractures (spinal compression)
b. muscle weakness
c. metabolic acidosis
d. n/v, constipation
e. insulin resistance
f. kidney stones

HYPERPARATHYROIDISM DIAGNOTIC TEST

a. PTH (INCREASED)
b. serum Ca (INCREASED)
c. serum phosphate
d. urine pH
e. bone density

TREATMENT OF HYPERPARATHYROIDISM

a. surgery
b. diuretics
c. meds that dec resorption of Ca from bone

HYPOPARATHYROIDISM

DECREASE in PTH, rare, seen after thryoid surgery, also with hypomagnesium

PATHO OF HYPOPARATHYROIDISM

dec in PTH causes dec in serum Ca levels

HYPOPARATHYROIDISM CLINICAL

a. muscle spasms
b. hyperreflexes
c. tetany
d. seizures
e. laryngeal spasms
f. dry skin, hair loss

HYPOPARATHYROIDISM DIAGNOSTIC

a. PTH level
b. serum Ca levels
c. serum phosphate level

TREATMENT OF HYPOPARATHYROIDISM

a. Ca supplements
b. Vit D

ADRENAL CORTEX FUNCTION (CORTICOSTEROIDS)

1. Glucocorticoids (Ex.cortisol)
2. Mineralocorticoids (Ex. aldosterone)
3. Androgens (Ex. testosterone and estrogen)

GLUCOCORTICOIDS

Glucose metabolism, role in response to stress
a. inc conversion of protein/fat to glucose
b. inc breakdown of protein
c. inc use of fatty acids
d. dec immune response

MINERALOCORTICOIDS

Fluid and e-lyte balance - aldosterone = sodium and water reabsorption and K excretion.

ANDROGENS

Sex steroids

CUSHINGS SYNDROME

EXCESS corticosteroids. Most common cause is ACTH secreting pituitary tumor. Other- adrenal tumor, ectopic ACTH producing tumor

PATHO OF CUSHINGS SYMDROME

No regulation, increase secretion of hormones. Always excess amounts of hormones

CLINICAL OF GLUCOCORTICOIDS

1. wt gain
2. glucose intolerance
3. protein wasting
4. easy bruising, purple striae in abdomen
5. bronze skin (melanocytes)
6. delayed wound healing
7. mood disturbances

CLINICAL OF MINERALOCORTICOIDS

1. water, Na retention, edema, loss of K+
2. HTN
**
ALDOSTERONE
****

CLINICAL OF ANDROGENS

1. acne
2. women - virilization (facial hair, masculine)
3. men - feminization

DIAGNOSTICS OF CUSHINGS SYNDROME

a. ACTH level (pituitary high) (adrenal low)
b. serum cortisol (high)
c. urine cortisol (high)
d. blood glucose

TREATMENT OF CUSHINGS SYNDROME

a. surgery (remove tumor)
b. meds to suppress cortisol

HYPERALDOSTERONISM

Occurs by itself excess secretion of aldosterone by adrenal gland.

PATHO OF HYPERALDOSTERONISM

Excess leads to inc Na and water reapsorption = hypovalemia. Also increase in secretion of K= hypokalemia

HYPERALDOSTERNISM CLINICAL

a. HTN
b. hypokalemia= cardiac dysrithmias

HYPERALDOSTERNISM DIAGNOSTIC

a.serum Na
b. serum K
c. serum aldosterone (HIGH)
d. aldosterone suppression test

HYPERALDOSTERNISM TREATMENT

a. surgery
b. meds to control HTN, hypokalemia

ADDISONS DISEASE

Insufficent function, all corticosteroids are dec. Etiology: autoimmune reaction

ADDISONS DISEASE PATHO

Elevated serum ACTH with inadequate corticosteroid synthesis. Adrenal tissue destroyed by antibodies against adrenal cortex

ADDISONS CLINICAL GLUCOCORTICOIDS

DECREASE LEVELS
1. dec in gluconeogenesis - hypoglycemia
2. weakness, fatigue
3. n/v
4. wt loss

ADDISONS CLINICAL MINERALCORTICOIDS

1. increase Na and water loss
2. K retention

ADDISONS CLINICAL ANDROGENS

1. dec axillarry/ pubic hair

DIAGNOSTICS OF ADDISONS DISEASE

a. serum cortisol and aldosterone (low)
b. urine cortisol and aldosterone (low)
c. ACTH (high)
d. serum K (high )
e. glucose (low)
f. ACTH stimulation tests

TREATMENT OF ADDISONS DISEASE

a. treat cause
b. replacement steroids
c. diet - in Na

PANCREAS- DIABETES MELLITUS

Lack or dec in insulin production by B-cells of pancreas or the insulin produced is ineffective.
Metabolic problems:
1. dec utilization of glucose:
2. increased fat mobilization:
3. increased protein utilization:

TYPE 1-IDDM (insulin dependent diabetes mellitus)

Insulin production dec or completely absent due to dec in number of B-cells in pancreas. <40 yrs old. Onset, progression of symptoms rapid
Patho: a. genetic factors., Human leukocyte antigens (HLAs)
b. autoimmune reaction.

TYPE 2- NIDDM (not insulin dependent diabetes mellitus)

80% of cases. >40 yrs. Amount of insulin produced may be normal, inc or dec. Problem -> insulin unable to bind with cell receptor sites. Due to a defect at receptor sites, dec # of sites or problem with postreceptor sites (inside cell). Onset of symptoms

CLINICAL OF TYPE 1

a. three P's - polyuria, polydipsia and polyphagia
b. weight loss or underweight status
c. ketosis

POLYURIA

increase urine

POLYDIPSIA

excessive thirst

POLYPHAGIA

increase appetite

DIAGNOSTIC TESTS OF PANCREAS DIABETES MELLITUS

1. blood glucose (sugar) level: (80-160)
2. fasting blood sugar: (70-110)
3. oral glucose tolerance test

TREATMENT OF PANCREAS DIABETES MELLITUS

1. diet
2. activity exercise
a. lowers blood sugar
b. improves insulin sensitivity
c. facilitates weight loss
d. reduces cholesterol and triglyceride levels

MEDS FOR TYPE 1

INSULIN

MEDS FOR TYPE 2

Oral hypoglycemic agents (OHAs)
a. lower blood sugar by stimulating B-cells to release insulin
b. make target tissues more sensitive to effects of insulin by inc # of receptor sites
c. enhance insulin's activity at post-receptor sites
d. dec glucose produ

DKA: TYPE 1 (diabetes ketose)

Glucose accumulates, use fat and protein stores. Fat -> ketones. Ketones -> metabolic acidosis and H2O loss. Protein metabolism -> further hyperglycemia. Hyperglycemia causes osmotic diuresis -> dehydration, hypovolemia and hyperosmolarity. Electrolyte im

HHNK (HYPERNOKITTITOCK): NIDDMS

like DKA except no ketosis. Severe hyperglycemia -> fluid and e-lyte loss -> hyperosmolarity, hypovolemia.
S&S: similar to DKA except no acidosis or ketosis
Treatment: same as DKA

HYPOGLYCEMIA

BS<50 symptoms
mild: tremors, palpitations, diaphoresis
moderate: impaired CNS function, HA, inability to concentrate, drowsiness
severe: disorientation, unconsciousness, seizures
Treatment: a. quick acting carbo
b. glucagon injection
c. high dextrose sol

RETINOPATHY

Chronic Complications/Prevention=
Deterioration of the blood vessels in the retina.

NEPHROPATHY

Chronic Complications/Prevention=Damage to capillaries that supply glomerulus. destruction of glomeruli and nephron damage -> renal failure

NEUROPATHY

Chronic Complications/Prevention=70% of diabetics. dec in nerve conduction
a. peripheral neuropathy: burning, aching, painful at times. muscle weakness, sensory loss, loss of fine motor skills, problems with ambulation. Potential for injury or undetected

MACROVASCULAR DISEASE

Chronic Complications/Prevention=atherosclerosis - CAD, stroke, peripheral vascular disease

INFECTION

Chronic Complications/Prevention=
a. sensory changes
b. hypoxia
c. pathogens
d. blood supply
e. WBC

NORMAL IMMUNE RESPONSE

A. Immunity: responsiveness to foreign substances. Functions:
1. defense (protects against invasion)
2. homeostasis
3. surveillance (removes mutations)

PROPERTIES OF THE IMMUNE RESPONSE

1. specificity: specific antibody for specific antigen
2. memory: remembers antigen
3. self-regulation: identifies own protein from foreign
4. self-limitation: immune response dec after antigen removed
5. specialization: reacts differently to various anti

TYPES OF IMMUNITY

1. natural: immune at birth
2. acquired
a. active: antibodies formed
b. passive: receives antibodies (quick less effective)

COMPONENTS OF THE IMMUNE SYSTEM

1. Lymphoid organs
a. central - bone marrow, thymus (B & T cells)
b. peripheral
2. mononuclear phagocyte system - monocytes, macrophages

HUMORAL IMMUNITY

Humoral Immunity: - antibody-mediated
1. B-lymphocytes: react with antigens, produce antibodies
2. immunoglobulins: antibodies
3. humoral response: B lymphocyte for antigen recognizes it and is activated -> secretes immunoglobulins -> destroys antigen

CELL MEDIATED IMMUNITY

1. t-lymphocytes:
a. t-cytotoxic - attack antigens
b. t-helper/t-suppresser
2. cytokines: factors secreted by T cells, B cells, monocytes, macrophages (messengers telling what to do)
3. macrophages: phagocytes
4. natural killer cells: large lymphocytes

ALTERED IMMUNE REACTIONS

Hypersensitivity Reactions
1. Type I: IgE-mediated: production of antigen-specific IgE after exposure to antigen. Large amounts of antigen and repeated exposures cause more IgE and sensitization. Further exposure = inflammatory response
2. Type II: tissue

ALTERED IMMUNE REACTION= ALLERGY

Type I - inc IgE leading to sensitization/inflammation

CLINICAL OF ALLERGY (MILD)

MILD=
a. sneezing
b. rhinitis
c. eyes
d. hives

CLINICAL OF ALLERGY (SEVERE)

SEVERE=
e. dysrhythmias
f. bronchial constriction
g. edema
h. hypotension

DIAGNOSTICS OF ALLERGY

a. skin tests
b. radioimmunosorbent (RIST) - total IgE
c. radioallergosorbent (RAST) - specific IgE.

TREATMENT OF ALLERGY

a. avoid allergen
b. desensitization
c. antihistamines
d. epinephrine

ALTERED IMMUNE REACTION= AUTOIMMUNITY (SLE)

body fails to recognize self-proteins and reacts against them

SYSTEMIC LUPUS ETYTHEMATOSUS (SLE)

chronic, systemic inflammatory disease of connective tissue

PATHO OF SLE

Production of autoantibodies against cellular components, main one is nucleic materials, DNA. Autoantibodies bind to DNA antigens and immune complexes accumulate - tissue damage

CLINICAL OF SLE

1. facial rash
2. photosensitivity
3. arthritis, joint pain
4. renal disorders
5. neurological disorders
6. anemia

DIAGNOSTIC OF SLE

1. antinuclear antibodies
2. Anti-DNA
3. anti Sm antibody (Smith nuclear antigen)

TREATMENT OF SLE

1. aspirin, NSAIDS
2. corticosteroids
3. immunosuppresives

ALTERED IMMUNE REACTION= ALLOIMMUNITY

Immune system produces reaction against tissues of another.
1. Transplant rejection: rejection due to reaction against antigens on donated tissue.

IMMUNODEFICIENCY DISORDERS

Immune system fails = recurrent infections
A. Congenital: genetic anomalies
B. Acquired : caused by another illness or related to:
1. nutrition
2. iatrogenic
3. trauma
4. stress

HIV/AIDS

AIDS caused by infection of HIV. Immune system becomes incompetent due to dec in T-cells = opportunistic infections.

TRANSMISSION OF HIV/AIDS

1. sexual transmission
2. contact with blood/blood products
3. perinatal

PATHO OF HIV/AIDS

HIV - retrovirus. HIV binds to CD4 receptors sites on cells. Genetic material enters cell and viral RNA is transcribed into DNA with reverse transcriptase. Viral DNA enters nucleus of cell and permanent part of cell's genetic structure. HIV infects T-cell

CLINICAL OF HIV/AIDS

1.Acute retroviral syndrome - seroconversion occurs, HIV antibodies develop. Flu-like symptoms. Symptoms occur 1-3 weeks after infection and last 1-2 weeks.
2.Early Infection - asymptomatic- median interval about 8 yrs. Vague symptoms
3.Early Symptomatic

DIAGNOSTICS OF HIV/AIDS

1. HIV antibodies
2. T-cell count
3. viral load

TREATMENT OF HIV/AIDS

1. monitoring
2.meds for HIV infection - block reverse transriptase, protease inhibitors
3.meds for opportunistic infections - treatment and prophylactic