Patho Exam 2

Posterior Pituitary

Hypersecretion ADH

• High levels of ADH with out physiologig stimuli
• Pituitary Surg
• Infectious pulmonary diseases
• Psychiatric disease after drug treatment

Thirst, dyspnea on exertions, fatigue, dulled consciousness, progressing abdominal cramps, vomiting, confusion and seizures

• Normal adrenal and thyroid function must exist
• Serum hypo-osmolarity and hyponatremis
• Urine hyperosmolarity

Posterior Pituitary

Hyposecretion of ADH

Insufficiency of ADH leading to polyuria and polydipsia

• Neurogenic
• Nephrogenic
• Psychogenic

• Insufficient amounts of ADH
• a lesion on hyopthalamus or posterior pituitary interferes with ADH synthesis, transport or release

• Inadequate response to ADH
• insensitivity of renal tubule to ADH, Kidney not responding

• Partial resistance to ADH
• Cause by an extremely large volume of fluid intake

Anterior Pituitary

Hyposecretion Any of the hormones

• Pituitary infarction
• Sheehan syndrome
• hemorrhage
• Shock
• Head trauma
• Infections
• tumors

All hormones are low

Target adrenal gland to release corisol

Cortisol deficeincy = decreased immunity

Target Thyroid gland

Thyroid deficiency= decreased metabolism (in children this makes them short)

• Target Gonads
• Loss of secondary sex characteristics, Gonadal failure, decreased fertility levels

Normal intelligence, short stature, obesity with immature facial features and puberty is often delayed

Giantism

Bones have already fused so results in Acromegaly

• Soft tissues grow
• Lowered protruding jaw
• Enlargement of heart
• teeth are splayed

Anterior Pituitary

Hypersecreation of Prolactin

hormonally active pituitary tumor

• amenorrhea (lose of mensies) galactorrhea (produce milk)
• hirsutism (male pattern hair growth)
• osteopenia (brittle bones)

hypogonadism, erectile sysfunction, impaird libido, oliospermia, diminished ejaculate volume

Hight than normal levels of TH

• Autoimmune
• abnormal stimulation of thyroid glad by IgG antibodies

skinny, alway shot, irritable, fatigue, exophthalmos

• death within 48 hours with out treatment
• symptoms hyperthermia, tachycardia, agitation, delirium, nausea, vomiting or diarrehea

Loss of thryoid tissue, decreased TH, Increas TSH and goiter

Loss of thyroid tissue- medication causes atrophy of tissue

Its a treatment for hyperthyroidism

person is heavier, sensitive to cold, lathargic

• common cause of preventable mental retardation
• appears normal at birth due to maternal TH

Results in cretinism- TH essential for normal breain development and growth

dwarfism, absent axillary and scant pubic hair, poorly developed breasts, pot belly, small umbilical hernia.

low TH excessive TSH

Hypothyroidism

nonpitting mucous edema

eye and facial puffiness Enlarged tongue

Due to a bacterial infection

Due to viral infection

Hashimoto disease

antibodies attack the TH

a combo of sub acute and Hashimoto- Can have auto antibodies that are triggered by a virus

occurs up to 6 months after delivery

is a medical emergency

hypothermia without shivering, hypoventilation, hypotension, hypoglycemia, and lactic acidosis

failure to synthesize adequate TSH

PTH

excess secreation of PTH from one or more parathyroid gland

• increase in PTH secondary to a chronic disease
• example renal failure

Function of parathyroid hormone is incease blood calcium.

The organ that makes the decision about how much calcium we need is the Kidney

If the kidney is in renal failure it constantly is thinking we need more calcium, sending a message to the PTH to release more calcium

• Hypercalcemia
• Bone resorption cause increased susceptibility to fracture
• Calcium stones

abnormally low PTH levels

parathyroid damang in thyroid surgery

• Hypocalcemia
• lowered nerve and muscle excitation
• spasms, hyper reflexia and clonic tonic convulsions

Bone deformities

the pancreas

More than one eleveated fasting plasma glucose level

Elevation plasma glucose levels in resposne to oral glucose tolerance test

classic symptoms of plydipsia, poly phagia and polyuria

Glycosylated hemoglobin (a lot of sugar in blood- glucose binds with hemoglobin)

Insulin Dependent Diabetes

lack of insulin and relative excess of glucagon

most commonly diagnosed in those younger than 18

beta cells destroyed due to autoantibodies

polydipsia and polyuria resulting from osmotic diuresis (glucose is attracting water to it) weight loss and polyphagia.

Ketoacidosis due to increase matabolism of fats and proteins

Non-Insulin Dependent

They do make insulin just done have the receptors to use it

Native Americans, Hispanics, black and alaskan natives

Most are over 40 and many are obese

• 3 main reasons why Type II
• Impaired Beta Cell Function
• Peripheral Insulin Resistance
• Increased Hepatic Glucose Production

Pancreas is making some insulin but is not making enough

Insulin can't bind;glucose can't go into cell stays in blood stream

Most common reason for Type II

liver doesn't know when to stop releasing glucagon released suger you don't need

Puritus, recurrent infections, visual changes, and parethesias

also plydipsia

because excess stress on pancreas and growing a baby increased sugar

family history of diabetes, high-risk ethnic group, advances maternal age, prior hx of GDM, overweight

• Hypoglycemis (insulin shock)
• Diabetic Ketoacidosis
• HHNK
• Somogyi Effect
• Dawn Phenomenon

90% are Type I

blood glucose of 46-60

pallor, tremor,anxiety, tachycardia, palpitations, diaphoresis(sweating), HA, Dizziness, fatiue, confusion, seizures, coma

Nervous system- Brain needs glucose for energy

Treatment- juice, fruit, candy bar

• Type I
• High sugar low insulin
• not enough insulin makes body release glucose more

• Slow onset
• metabolic acidosis producing ketone bodies
• Thirsty, confusion, fatigue

Alot of urine

Type II

• Slow onset
• High mortality due to high serum glucose (More than 500) leading to sever dehydration

Treatment: manage fluid/electrolytes and glucose control

Older adults who binge on sweet and didn't adjust meds

combination of hypoglycemia follwed by rebound hyperglycemia

Startes with Hypo but body kicks in a raises glucose/stress hormone ends up in hyper

early morning rise in blood glucose with no hypoglycemia during the night due to nocturnal elevation of GH

GH increases blood sugar in the night= high morning blood sugar

due to capillary basement membrane thickening, ischemia hypoxia

blood vessel changes and RBC aggregation

Increase sugar= retina vessels rupture= blindness

More likely in Tpe II as a result of Hyperglycemia

end stage renal disease

Type I

proteinuria

Coronary Artery Disease (most common cause for death in Type II)

Stroke (2x as common with diabetics)

Peripheral Vascular Disease (PVD) due to occlusions of small vessels (may result in gangrene in lower extremities)

increased risk due to senses impairment (don't know you have a cut)

WBC can't function right when there is too much sugar

poor circulation

microbes love sugar so they increase in number

Adrenal cortex

Excessive level of cortisol

excessive anterior pituitary secreation of ACTH

• Altered fat metabolism -Moon face and buffalo hump
• Muscle weakness due to protein breakdown
• deranged glucose metabolism
• susceptibility to infection

hypertension, renal potassium wasting, hypokalemia, and neuromuscular manifestations

addison's disease

Addison disease is caused by autoimmune mechanisms that destroy adrenal cortical cells and is more common in women.

Feminizations- boys become girl like

Virilization- girls become boy like

Acromegaly

graves disease

HHNKS

Type I Diabetes mellitus

Type II diabetes

SIADH

Dawn Phenomenon

A. dwarfism

acromegaly

d. polyuria

B. constipation

D. myxedema coma

D. all of the above

a. mental retardation

C. increased ostoclastic activity

E. tetany

D. anterior pituitary adenoma

C. thyroxine

D. insulin shock

C. type I diabetes