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
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ALDOSTERONE
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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