Patho Quiz 2 Review

Chapter 13:

Syndrome of Inappropriate Antidiuretic Hormone (SIADH)

What is it?

o Inappropriate production & release of ADH despite the changes in osmolality and blood

volume.

RF:

o Tumor that releases ADH

o Water in the cells = increase in total body water & causes sodium dilution

S/S:

o Serious = psychosis, coma, seizure, gait changes

o Hypotonic Hyponatremia

o Anorexia, N/V

o Muscle cramps & weakness

o Sodium concentration

Dx:

o Hyponatremia (<135)

o High concentrated urine with high sodium

Tx:

o Isotonic or hypertonic saline IV (hypertonic IV is used for hyponatremia and changes in

mental status)

o Remove the cause

o Water restriction (to prevent excess fluid build-up in body)

ADH (or vasopressin) = hypothalamus -> posterior pituitary gland

o Regulates water absorbed in the kidneys.

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Diabetes Insipidus

What is it?

o Insufficient ADH

o Body cannot concentrate and retain urine

Causes?

o Inadequate kidney response to ADH

o Insufficient production & secretion of ADH

o Water intoxication

S/S:

o Polyuria
 o Polydipsia (excessive thirst) = dehydration

o High amounts of dilute urine

o High serum osmolality

o Shock and death (if not treated)

Dx:

o History of brain tumor removal, cranial surgery, or head trauma

o Labs: serum solute concentration, ADH levels, urine specific gravity

Tx:

o Fluids to replace urine

o Hypotonic IV

o Desmopressin (antidiuretic med.)

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Hyperthyroidism

What is it?

o Autoimmune disease that causes overstimulation of the thyroid gland leading to

excessive thyroid hormone secretion.

o Common cause: Graves disease

o Thyrotoxic crisis (thyroid storm): sudden serve worsening of hyperthyroidism that can

cause death.

S/S:

o Weight loss
 o Agitation/restlessness

o Tremors

o Sweating/heat intolerance

o Tachycardia/palpations

o Irregular periods

o Exophthalmos (bulging eyes)

o Goiter (enlarged thyroid gland)

Dx:

o TSH levels

o Elevated T3 and T4 levels

o Increased radioactive iodine by thyroid

Tx:

o Gland destruction via radioactive iodine

o Surgical removal (Full removal = Oral thyroid hormone (Levothyroxine))

Hypothyroidism

What is it?

o Deficient thyroid hormones

o Congenital (underdevelopment) or acquired (Need neonatal screening for congenital)

o Acquired: destruction of gland, impaired hormone synthesis or excretion

o Hashimoto thyroiditis: autoimmune hypothyroidism that destroys the thyroid.

o Iodine deficiency

o Surgical removal or radiation of thyroid

S/S:

o Lethargic/weakness/fatigue

o Cold intolerance

o Weight gain

o Dry skin/course hair

o Goiter to help with function

o Impaired memory & reproduction

Dx:

o Elevated TSH levels

o Low T3 and T4

o Thyroid antibodies present

Tx:

o Replacing and normalizing levels of thyroid hormones

o Levothyroxine (Synthroid)
Cushing Syndrome

What is it?

o Prolonged exposure to elevated cortisol or glucocorticoids secreted by the adrenal cortex

or from taking steroid medications.

Causes?

o Long term corticosteroid use (prednisone)

o Tumors in the pituitary gland stimulating excess Adrenocorticotropic hormone (ACTH)

production.

o Tumor of the adrenal gland stimulating cortisol production

o Production of stimulating hormones from a distant site (lung cancer)

S/S:

- Suppression of immune response/poor healing

- Moon face// buffalo hump (face fat and upper back fat)

- Striae

- Osteoporosis

- Glucose intolerance = diabetes

- Hirsutism

- Hyperglycemia

- CNS irritability

- Edema

- GI distress – increase in acids

- Increased susceptibility to infection

Females: amenorrhea, hirsutism, think skin, purple striae, bruises & petechiae (tiny spots of

bleeding under the skin)

Dx:

- 24-hr urine collection showing elevated cortisol excretion

- Imaging to see tumors

Tx:

- Surgery/radiation

Addison Disease

What is it?

o ACTH deficiency

o Insufficient production of cortisol and aldosterone

o Destruction of the adrenal cortex layers

S/S:

- Hyperpigmentation (bronze pigmentation of skin)

- Hyponatremia/Hyperkalemia

- Hypotension/shock

- Changes in hair distribution

- Weight loss

Adrenal Crisis = profound weakness, dehydration, vascular collapse (low BP), Renal shut

down.

Dx:

- Low NA

- High K

- Low corticosteroid levels

Tx:

- Isotonic IV fluid replacement with hydrocortisone

- PO glucocorticoids & mineralocorticoids for life

Hypothalamic-pituitary axis

- Controls synthesis and secretion of hormones

- Hypothalamus = releases hormones to act on pituitary gland; pituitary then respond by

either releasing it or stimulating another endocrine gland to release it.

Feedback Mechanisms:

- When above normal range = production & secretion is slowed

- When below normal range = production & secretion increases

o Autonomic Nervous System (ANS): fight or flight

o Cerebral Cortex: cognitive activities such as focus and attention

o Limbic system: emotions (fear, anger, anxiety)

o Thalamus: sensory input (smell, hear, vision, touch)

o Hypothalamus: releases hormones that act on the ANS

o Reticular activating system: increased alertness & muscle tension & stimulated ANS.

ANS:

- Increased BP, HR, & RR

- Dilated pupils

- Pale of flushed skin

- Trembling

- Increased blow flow to heart/lungs/muscles

- Gastric function decreased to shunt vital body organs

Hormonal Response to Stress:

1. Releases Corticotropin-releasing hormone (CRH) which then stimulates the pituitary to

secrete ACTH.

a. Adrenal glands release cortisol, which is needed to increase metabolism, regulate

blood glucose for energy, & anti-inflammatory properties.

a. Neurological response from certain organs

b. Ex: blood shunted to vital organs = increase in vital signs & alertness

General Adaptation Syndrome (GAS)

- Neuroendocrine response

3 stages:

1. Alarm stage

- Catecholamines and cortisol’s released

- Fight or flight (prepares body for defense against stressor)

- ADH is increased to retain fluid to keep BP up

- GH, thyroid hormones, & reproductive hormones are low

2. Resistance Stage

- Persistent stress

- Cortisol levels drop (negative feedback)

- Cortisol release over time = exhaustion of immune and inflammatory response

- Negative affect of growth, metabolism, and reproduction

- Increased ADH levels = excessive fluid retention = hypertension

3. Exhaustion Stage

- Chronic stress

- Energy depletion
 - Degeneration of cells, tissues, and organs

- Poor health and loss of homeostasis

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Chapter 20:

Diabetes Mellitus

What is it?

o Inability to regulate glucose = inadequate metabolism of macronutrients.

o 2 types

Type 1: cannot produce insulin

- Absolute deficit of insulin

- Cell-mediated immune-destruction of beta cells in pancreas

- Hyperglycemia, hyperketonemia, ketoacidosis

S/S:

- Polydipsia

- Polyuria

- Polyphagia (excessive hunger)

- Nocturia (walking up at night to pee)

- Lethargic

- Blurred vision
Dx:

§ Blood glucose levels

o Fasting >126 mg/dL

o Random >200

§ Urine analysis: ketones, glucose

§ Glycosylated hemoglobin: > or equal to 8%

Tx:

- Glycemic control (glucose 70-120)

- Carbohydrate intake

- Insulin replacement therapy

Type 2: doesn’t produce enough or doesn’t respond well to insulin

- Insulin resistance (reduced tissue sensitivity)

- Reduction in adequate insulin secretion

RF:

- Obesity

- Age > 30

- Native Americans, Hispanics, African Americans

S/S:

- Visual changes and kidney function

- Peripheral vascular disease

- Neuropathy

- Recurrent infections

Dx:

§ Blood glucose levels

o Fasting >126 mg/dL (“pre”: 110 to 125)

o Random >200

Tx:

- Weight control

- Oral glycemia agents

- Insulin replacement therapy

- Goal: maintain blood glucose levels

Gestational Diabetes

What is it?

o Glucose intolerance with onset during pregnancy (Think Gestational = Glucose)

o Can lead to type 2

o Untreated = fetal macrosomia, hypoglycemia, hypocalcemia, birth defects

- Hypoglycemia

o Excessive insulin dose

o Unbalanced food intake or vomiting

o Strenuous exercise = infection

- Diabetic Ketoacidosis

- Hyperglycemia hyperosmolar nonketotic syndrome (HHNK) = problem with type 2

diabetes where blood sugar levels remain high (hyperglycemia, high plasma osmolality,

dehydration, lack or mild ketosis, changes in level of consciousness)

- Somogyi effect (hyperglycemia as a reaction to insulin-induced hypoglycemia) & dawn

phenomenon (an individual’s blood glucose level upon waking is higher than before they

went to bed)

Chronic Complications Type 1:

- Microvascular

o Retinopathy (eyes)

o Nephropathy (kidneys)

- Macrovascular

o Vascular disease

o Coronary artery
 o Cerebrovascular

o Peripheral

- Neuropathies

o Nerve degeneration

o S/S = numbness/tingling, weakness/muscle wasting, & pain

- Infection

Chronic Complications Type 2:

- Autonomic neuropathy

o Dizziness and syncope

- Eyes: glaucoma, retinopathy, cataracts

- Atherosclerosis

o Ischemic heart disease

o Myocardial infract

o Peripheral vascular disease

- GI motility: delayed gastric emptying; diarrhea, constipation

- Bladder stasis & infection, ED

- Gangrene

- Hypertension

- Microangiopathy

o Cerebral infarcts

o Hemorrhage

- Neuropathy
 o Kidney disease

o Glomerulosclerosis

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Diabetic Ketoacidosis:

- Problem of deficient insulin and severe hyperglycemia leading to metabolic acidosis.

- Type 1 diabetes (demand for insulin)

S/S:

- 3 P’s presence with ketones, dehydration, and fatigue

- Fruity breath

- Glucosuria (presence of glucose in the urine)

- Kussmal’s breathing

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Hypoglycemia: low blood sugar (type 1

S/S:

- Weakness

- Pallor or cool/clammy skin

- Neuroglycopenia (glucose deprivation in the brain)

- Adrenergic symptoms

- Poor concentration

- Extreme hunger

- Blurred vision
 - Dizziness

- Confusion

- Dysphasia

- Lack of coordination

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Insulin

- Anabolic hormone

- Required for uptake of glucose in cells (live, muscle, and adipose cells)

- Promotes protein synthesis/stores lipids

Pancreas:

Endocrine

- Insulin

- Glucagon

Exocrine

- Digestive enzymes

- Alkaline fluids

Islets of Langerhans

- Alpha, beta & delta cells