Exam 4 part 2 Flashcards

Question

Subluxation

Answer 1

- Injury which occurs when contact between opposing joint surfaces is only partially lost * **Can be AQUIRED, there is PAIN, @ joint-may need REDUCTION

Answer 2

Ligament tear--wrist, ankle, knee most common areas

Answer 3

Tearing or stretching of a muscle or tendon

Answer 4

Complete separation of tendon or ligament from bony attachment site. Young athletes, distance runners STAGING- 1ST--3RD Degree--1st Least 3rd Complete Avulsion ****Determines therapy and treatment ****The larger the injury--the more chance to REINJURE

Answer 5

Painful inflammation of tendons (Tendonitis) | Most common form of Epicondylopathy

Answer 6

result of Tendonitis - Medial : also know as the Golfers elbow. Is the result of forces affecting the forearm muscles responsible for forearm flexion and pronation - Lateral : also know as Tennis elbow. Is caused by irritation and overstretching of the extensor carpi radialis brevis tendon and forearm extensor muscles resulting in tissue degradation. S &S : Localized to one side of the joint, local tenderness and more pain with active motion rather than passive movement

Answer 7

is the painful inflammation of the Bursae; Bursae are small sacs lined with synovial membrane and filled with synovial fluid that are located between bony prominences and soft tissue, such as : tendons, muscles, and ligaments Common in the shoulder, Hips, and Elbows It is important when diagnosing and treating Bursitis to make sure that there is no infection in the Bursa. If so… S & S would be pain, Redness, and low grade fever

Answer 8

Rapid breakdown of muscle that causes the release of muscle cell contents (including myoglobin) into extracellular space and bloodstream. Possibly caused by physical interruptions in the muscle (sarcolemal) membrane.

Answer 9

-Delta lesions in membrane release cellular contents. Relatively rare, but has many causes and can cause serious complications: -Hyperkalemia (due to release of intracellular potassium into circulation) -Metabolic acidosis (due to release of intracellular phosphorus and sulfate) -*Acute renal failure (because myoglobin precipitates in the renal tubules, obstructing flow and producing injury) -Disseminated intravascular coagulation (DIC) (Sarcolemma damage starts the clotting cascade) *Most important complication

Answer 10

Classic Triad of symptoms: Muscle pain Weakness Dark urine/myoglobinuria Along with the release of myoglobin, creatine kinase and other serum enzymes are released in massive quantities. Loss of potassium/phosphate/nucleotides/creatinine/creatine

Answer 11

Compartment syndrome is increased pressure within one of the body's compartments which contains muscles and nerves. Compartment syndrome occurs after a traumatic injury or as a result of any condition that can increase compartment content such as a car crash, bone fracture, edema, or infarction. The trauma causes a severe high pressure in the compartment which results in insufficient blood supply to muscles and nerves.

Answer 12

The major signs and symptoms are the five P’s: 1. Pain (out of proportion to the injury) 2. Pallor 3. Pulse decline 4. Pressure Increased 5. Paresthesia. The weight of a limp limb could generate enough pressure to produce muscle ischemia.

Answer 13

It is a rare genetic disorder of the muscles. It is most common in children and adolescents. It is caused by a hyper metabolic reaction to certain anesthetics or succinylcholine (depolarizing muscle relaxants). The body reacts with an altered or prolonged release of intercellular calcium.

Answer 14

- Hypermetabolism: Extremely high body temp - muscle rigidity - rhabdomyolysis - sinus tachycardia - respiratory acidosis - masseter muscle spasm/muscle contractions.

Answer 15

“porous bone”. Metabolic disease. Old bone is being resorbed faster than new bone is being made. This progresses slowly until fracture (fx) occurs. A bone density test of 2.5 or more below standard is indicative of osteoporosis. Can be total skeleton or just a segment.

Answer 16

``` genetics fair, pale decrease in calcium intake caucasian sedentary life-style decrease in vitamin D intake age smoking female early menopause small, thin increase alcohol consumption ```

Answer 17

``` Osteoporosis develops when remodeling cycle is disrupted. Bone resorption (osteoclasts) increases. Bone formation (osteoblasts) decreases. ```

Answer 18

Depends on bone, pain, bone deformity -> advanced stage, Kyphosis “hunchback” -> vertebral bone collapse.

Answer 19

“softening of the bone” Normal amount of collagen but not enough calcium, bone volume is unchanged. This is caused by a Vitamin D deficiency.

Answer 20

- pain in musculoskeletal system - pain particularly in hips - waddling gait - bowed legs or “knock knees” - **low back pain earliest complaint may start in 20’s - pain in ribs/feet/vertebral column

Answer 21

Also called “osteitis deformans”; it is a state of increased metabolic activity in the bone and is an abnormal & excessive bone remodeling (both resorption and formation)

Answer 22

- Begins with excessive breakdown of bone - Results in laying down of unorganized bone - Trabecular network diminishes (this network is the support structure of the bones) - Bone marrow is replaced by extremely vascular fibrous tissue - Formation of abnormal new bone at accelerated rate

Answer 23

Evident in skull first (it thickens and assumes asymmetric shape) - deafness - sensory deficits - dementia and HA - all d/t increased pressure on brain created by thickened portions - stress fractures in lower extremities d/t decrease in trabecular network

Answer 24

a bone infection most often caused by bacteria; however, fungi, parasites and viruses also can cause bone infection. It is a common complication of sickle cell anemia and low oxygen tension. Regardless of the source of the pathogen, the pathologic features of bone infection are similar to those in any other body tissue.

Answer 25

vary with the age of the individual, the site of involvement, the initiating even, the infecting organism, and the type of infection - acute, subacute or chronic.

Answer 26

causes abrupt onset of inflammation. If an acute infection is not completely eliminated, the disease may become subacute or chronic.

Answer 27

subacute osteomyelitis, signs and symptoms are usually vague. In the chronic stage, infection is indolent or silent between exacerbations.

Answer 28

an infection that enters from outside the body, for example through open fractures, penetrating wounds, or surgical procedures.

Answer 29

caused by pathogens carried in the blood from sites of infection elsewhere in the body.

Answer 30

( a common form of osteomyelitis) is usually found in infants, children and elderly persons. Microorganisms reach the vertebrae through arteries, veins, or lympathic vessels.

Answer 31

· Chronic, systemic, inflammatory autoimmune disease | · Joint swelling and tenderness and destruction of synovial joints

Answer 32

Cartilage damage in RA is result of 3 processes 1. neutrophils & other cells become activated degrading articular cartilage 2. enzymatic breakdown of cartilage and bone 3. synovium converted into pannus

Answer 33

· Onset usually insidious · Begins with general systemic manifestations of inflammation · Fever, fatigue, weakness, anorexia, weight loss, generalized aching and stiffness · Local manifestations appear gradually · Joints become painful, tender, and stiff · Pain early in disease caused by pressure from swelling · Late pain is caused by sclerosis of subchondral bone and new bone formation

Answer 34

· Common age related disorder of synovial joints · Local areas of loss & damage of articular cartilage · New bone formation of joint margins · Thickening of joint capsule

Answer 35

Primary defect is loss of articular cartilage Cartilage becomes thin and absent in some areas Unprotected bone becomes sclerotic (dense & hard)

Answer 36

· Appear in 5th or 6th decade of life · Pain in one or more joints with weight bearing, use of the joint, or load bearing · Resting the joint relieves pain · Stiffness in joints · Enlargement or swelling of joints · Tenderness · Limited ROM · Paresthesias (numbness, tingling)

Answer 37

- Chronic inflammatory joint disease - It is a systemic autoimmune disease - Characterized by stiffening and fusion (ankylosis) of the spine and sacroiliac joints

Answer 38

- AS begins with inflammation of fibrocartilage in cartilaginous joints - first affects the sacroiliac joint Inflammatory cells infiltrate the fibrous tissue of the joint capsule, eroding bone and fibrocartilage - this leads to repair of the bone, over and over again, leading to ossified scar tissue - this then causes joints to fuse or lose flexibility

Answer 39

- Low back pain and stiffness - Worse after prolonged rest and alleviated by physical activity - Early morning stiffness

Answer 40

- Gout is a syndrome caused by incomplete purine metabolism, resulting in excess serum uric acid levels (hyperuricemia) - Characterized by inflammation and pain of the joints - Caused by either excessive uric acid production or underexcretion of uric acid by kidneys

Answer 41

- linked to purine metabolism and kidney function - Crystals of Uric acid are formed and then deposit into the joints - Urate excretion from the kidneys slows down

Answer 42

- Primary symptom is severe pain - Hyperuricemia - recurrent abrupt attacks at a single joint (typically the big toe) - joint becomes hot, red, and extremely tender. Can be swollen. Usually at night. - deposits of tophi in and around the joints - renal disease - renal stones 50% are in big toe; other joints affected can be- heel, ankle, knee, wrist, elbow

Answer 43

Diffuse pain, fatigue, increased sensitivity to TOUCH Chronic Musculoskeletal SYNDROME

Answer 44

Genetic factors Alterations in genes affecting serotonin, catecholamines, and dopamine these are stress receptors and sensory processing due to stress triggers

Answer 45

- Diffuse, chronic pain - CONFIRMATION-TENDERNESS IN 11 OF 18 TENDER POINTS - Burning or gnawing pain - NO systemic process - Anxiety & Depression- Difficult to diagnose

Answer 46

Most common malignant bone forming tumor

Answer 47

2nd most common tumor; middle aged or older and peaks in the 6th decade of life; cartilage forming tumor (chondroid cartilage) ; Giant cell tumor that can grow rapidly

Answer 48

Most common Collagenic tumor producing fibrous connective tissue and can affect bone or soft tissue( collagen forming tumor) ; Most common in the Femur or Tibia

Answer 49

6th most common primary bone tumor; It is generally benign but can become malignant after radiation treatment. Wide age range but normally not below 10 years old or over 70 years old ( mostly btwn 20-40 yrs olds are diagnosed) and tend to affect Females more often than males. It is a solitary , circumscribed tumor that causes bone resorption bcs of its osteoclastic origin - located in the center of the epiphysis in the femur, tibia, radius, or humerus. S & S - pain, local swelling, and limitation of movement

Answer 50

Rare benign tumor of the muscle that generally occurs in the tongue, neck muscles, larynx, uvula, nasal cavity, axilla, vulva, or heart. highly malignant and metastasizes rapidly; common in infants, children, and teenagers and located in the muscle tissue of head, neck and genitourinary tract with remainder found in the trunk and extremities.

Answer 51

Produced in posterior pituitary. Excess amounts of this hormone results in water retention and a hypoosmolar state, where as deficiencies in the amount or response to ADH result in serum hyperosmolarity.

Answer 52

Characterized by high levels of ADH without normal physiologic stimuli for its release. Caused by: - Ectopic production of ADH by tumors and cancers in other areas of the body - Surgery (causes temporary SIADH) - Pulmonary and CNS disorders - Medications

Answer 53

Enhanced water retention due to increase of ADH. ADH increases renal collecting duct permeability to water which increases water reabsorption by the kidneys. Sodium in body serum is diluted, causing hyponatremia and urine that is inappropriately concentrated

Answer 54

``` Manifestations of hyponatrimia: mild: Thirst Impaired taste Anorexia Dyspnea on exertion Fatigue Dulled senses moderate: GI problems (vomiting/cramps) severe: Confusion Lethargy Muscle twitching Convulsions Neurologic damage ```

Answer 55

Characterized by insufficient activity of ADH, leading to polyuria (frequent urination) and polydipsia (frequent drinking) Two major causes: Neurogenic: Caused by the insufficient secretion of ADH. Occurs when any organic lesion of the hypothalamus, pituitary stalk, or posterior pituitary interferes with ADH synthesis, transport, or release. Well recognized complication of closed head injury Nephrogenic: Caused by inadequate response of the renal tubules to ADH, which is usually acquired or genetic. Related to damage of the tubules by drugs or disorders.

Answer 56

Partially or total inability to concentrate urine. Large volumes of diluted urine leading to plasma osmolarity. As water is lost in the urine, serum hypernatremia and hyperosmolarity occur.

Answer 57

- Polyuria/nocturia - Continuous thirst and polydispia - Long term patients will develop large bladder capacity and hydronephrosis

Answer 58

A condition of the anterior pituitary. It is the absence of one or more SELECTED hormone (TSH, FSH, LH, TSH, ACTH, or GH). Some possible injuries of the pituitary include vascular infarction, aneurysm, tumor, or any other condition that would impede secretion.

Answer 59

``` Cold Intolerance Skin Dryness Mild Myxedema Lethargy Decreased Metabolic Rate ```

Answer 60

Loss of sex drive Women: Loss of period Atrophy of uterus Men: testicles smaller Less Hair

Answer 61

``` Loss of Cortisol-Life threatening w/I 2 weeks Nasuea/Vomiting Anorexia Fatigue Weakness Hypoglycemia Decreased Aldosterone secretion Decreased urine output ```

Answer 62

``` Adults: Fatigue Social Withdraw Loss of Motivation Osteoporosis Altered Body Composition Children: Dwarfism ```

Answer 63

A condition of the anterior pituitary. It is the hypersecretion of various hormone(s) of the pituitary. It is usually due to local invasion of a pituitary tumor (adenoma).

Answer 64

The manifestations vary according to tumor growth and the hormone that is being secreted. Most commonly we see neurological symptoms such headaches, fatigue, neck pain, stiffness, and visual changes. The pressure of the tumor could result in thyroid and adrenal hypofunction leading to symptoms of hypothyroidism and hypocortisolism.

Answer 65

Low levels of all the anterior pituitary hormones. - All hormones of the anterior pituitary gland are deficient. (TSH, corticotropins, Substance B and Prolactin). - cortisol deficiency from lack of ACTH, potentially life threatening. - thyroid deficiency from lack of TSH, rare, cold intolerance, skin dryness, mild myxedema, lethargy and decreased metabolic rate. - loss of secondary sex characteristics from lack of follicle-stimulating hormone FSH

Answer 66

These tumors are very small... cellular and are unique to the types of cells they originate from. - Hypersecretion of that hormone - Surrounding cell types will get pinched off and decreased Manifestations occur due to cell changes as well as swelling. - Headaches - Fatigue - Stiff neck - Visual changes - Neuro changes

Answer 67

Hypersecretion of growth hormone (Acromegaly) occurs d/t continuous exposure to the growth hormone (GH) and insulin like growth factor 1; also d/t GH-secreting pituitary adenoma

Answer 68

In GH secreting adenomas, the usual GH baseline secretion pattern and GH sleep-related GH peaks are lost; secretion of GH is never completely suppressed; GH secretion occurs at all times of day and is unpredictable; if this happens in children whose epiphyseal plates have not yet closed, it’s called giantism (not acromegaly), where skeletal growth is excessive; if this happens in adults, it causes connective tissue proliferation and increased cytoplasmic matrix as well as bony proliferation.

Answer 69

* Hypertrophy of sweat and sebaceous glands * Course skin/hair * Cardiomegaly/hypertension * Sexual dysfunction * Peripheral neuropathy * Visual field deficits * Large nose , jaw, tongue * Enlargement bones on face, hands and feet. Lower jaw protrudes. Prominent supraorbital ridge. Barrel chest. * Abnormal glucose tolerance (diabetes mellitus) S & S * Arthritis * Skeletal growth is excessive * Renal tubules resorption of phosphate

Answer 70

- Results from an increased level of Thyroid Hormones (TH) - Graves disease is most common cause-- 50-80% of cases - higher incidence in women

Answer 71

- Results from type II Hypersensitivity where there is a stimulation of Thyroid autoantibodies directly against the TSH receptor - stimulation of these autoantibodies, called thyroid-stimulating immunoglobulins (TSIs), stimulate the TSH receptors on the thyroid gland and result in hyperplasia (Goiter) - This leads the thyroid to continue producing TH, leading to an increase in TH in the body and s/s of hyperthyroidism - TSH is also inhibited through a negative feedback to the pituitary - the pituitary senses too much TH in the body, so it does not produce and release TSH

Answer 72

* *Opthalmopathy (think of EYE PROBLEMS) * *exopthalmos- protrusion of the eyeballs * Also think of INCREASED metabolic rate and increased sensitivity - Tachycardia, diarrhea, warm skin, hyperreflexia - enlarged Thyroid just think of “eyes”

Answer 73

deficient production of TH by the thyroid gland LOW TH levels with HIGH TSH -loss of thyroid function leads to decreased production of TH and increased secretion of TSH & TRH - Primary thyroid malfunction- when the thyroid is dysfunctional--resulting in low TH & High TSH - secondary thyroid malfunction- when the pituitary, and thus secretion of TSH, is dysfunctional (rare)

Answer 74

**Myxedema- nonpitting, boggy edema, especially around the eyes, hands and feet (puffy face) DECREASE in Metabolism and energy - Bradycardia - Constipation

Answer 75

- RARE, EMERGENCY- DEATH within 48 hours when not treated - Occurs in patients who are undiagnosed or partially treated hyperthyroid ds Causes: -excessive STRESS, such as Infection, CV and pulmonary disorders, trauma, seizures, emotional distress. MANIFESTATIONS: hyperthermia, atrial tachydysrhythmias, heart failure, agitation, nausea, vomiting, diarrhea leading to dehy, delirium/agitation

Answer 76

- hyperthermia - atrial tachydysrhythmias - heart failure - agitation - nausea - vomiting - diarrhea leading to dehydration - delirium/agitation ******#1 Problem Cardiac #2 Problem Dehydration

Answer 77

a) Medical emergency b) Decreased LOC, hypothermia w/o shivering, hypoventilation, hypotension, hypoglycemia and lactic acidosis c) High Risk: older patients with severe vascular disease and with moderate or untreated hypothyroidism. May occur after overuse of narcotics or sedatives or post acute illness.

Answer 78

``` - Hypothermia without shivering · Hypoventilation · Hypotension · Hypoglycemia · Lactic Acidosis ```

Answer 79

Greater than normal secretion of parathyroid hormone (PTH) and hypercalcemia. Classified as either primary or secondary. Causes: - Parathyroid adenomas (most common) - Parathyroid hyperplasia - Parathyroid carcinoma - Genetic causes

Answer 80

Primary: Characterized by inappropriate excess secretion of PTH by one or more of the parathyroid glands. PTH secretion is increased and is not under usual feedback control mechanisms. Calcium level in the blood increases because of increased bone resorption and GI absorption of calcium.

Answer 81

Secondary: Response of the parathyroid glands to chronic hypocalcemia, which can be associated with decreased renal activation of Vit D. Secretion of PTH is elevated, but it can’t achieve normal calcium levels due to deficiency of vitamin D.

Answer 82

- Hypercalcemia/hypophosphatemia **Hallmark** - Pathological facial muscular problems - Headache - Nausea and vomiting - Fatigue - Depression - Anorexia - Kidney stones

Answer 83

Abnormally low PTH levels. Causes: - Damage to the parathyroid glands during thyroid surgery (most common) - Genetic syndromes - Hypomagnesemia - Autoimmune

Answer 84

Lack of circulating PTH causes depressed serum calcium levels and increased serum phosphate levels. In the absence of PTH, resorption of calcium from bone and regulation of calcium reabsorption from the renal tubules are impaired.

Answer 85

``` -Hypocalcemia/hyperphosphatemia **Hallmark** Manifestations due to low calcium levels in blood: Dry skin Hair loss Hypoplasia of developing teeth Horizontal ridges on nail Cataracts Bone deformities Basal ganglia calcification ``` ``` Low threshold of nerve excitement: Tetany: muscle spasms Hyperreflexia Clonic-tonic seizure Laryngeal spasms +Chovstek and +Trosseau signs ```

Answer 86

The stomach converts food/carbs into glucose, the glucose then enters the bloodstream. The pancreas normally releases insulin in response. The insulin and the glucose can then enter the cells together. In a fast or when you skip a meal, your liver pumps out glucose to meet the needs of your cells and body.

Answer 87

Insulin dependant In Type 1, the cells that produce the insulin (Beta Cells) were damaged or destroyed by a T-Cell autoimmune disease. The cause varies but there are several contributing factors including genetics, viruses, drugs, and or illness. The Beta Cells were damaged so the pancreas makes little to no insulin. What is produced enters the bloodstream but it’s not enough. The glucose cannot enter the cells without the insulin therefore it builds up in the blood stream.

Answer 88

Insulin resistant In type 2, the Beta Cells are fine therefore sufficient amounts of insulin are being produced. The defect is with the cellular receptor; the cell does not recognize the insulin and therefore does not let the insulin or glucose in. It is insulin resistant. Therefore you still end up with low intracellular glucose. In response, the pancreas thinks the cells are starving and compensates but continually pumping out insulin and eventually fails due to overproduction. Once again, we have a backup of glucose and now insulin in the bloodstream.

Answer 89

Autoimmune: Genetic or environmental factors. Whites have 1.5-2 times higher risk than non-whites.

Answer 90

Obesity, high fat and cholesterol levels, high blood pressure, smoking, sedentary lifestyle, over 30 years of age, race (highest risk for black and native Americans)

Answer 91

3 P’s: Polydipsia: Increased Thirst related to intracellular dehydration. Polyuria: Increased Urination due to hyperglycemia Polyphagia: Increased Hunger due to cellular starvation - Prolonged wound healing due to impaired blood supply - Visual Changes/Blurry Vision due to elevated blood glucose levels - Cardiovascular Symptoms: Chest Pain due to diabetes contribution to formation of atherosclerosis affecting circulation. - Paresthesisas: Numb or tingling hands/feet - Weight Loss due to fluid loss and loss of tissue as fat and proteins are used for energy - Fatigue due to poor use of food products - Recurrent Infections-Yeast loves sugar - Rapid Onset - Genital Pruritus due to fungal growth

Answer 92

``` Nonspecific: Polydipsia: Increased Thirst Polyuria: Increased Urination Recurrent Infection-Yeast loves sugar Pruritus: Itching Visual Changes/Blurry Vision Neuropathy Symptoms Paresthesisas: Numb or tingling hands/feet ```

Answer 93

- Hypoglycemia - Ketoacidosis (DKA) - Hyperosmolar hyperglycemic non-ketotic syndrome (HHNKS) - Somogyi effect - Dawn Phenomenon

Answer 94

(<70) (extra insulin from not eating when taking insulin meds) S/S: pallor, tremor, anxiety, tachycardia, palpitations, hunger, poor judgement, seizure/coma, DRUNK ACTING.

Answer 95

(DKA) more common in Type I. S/S: metabolic acidosis, postural dizziness, CNS depression, anorexia, nausea, abdominal pain,thirst, polyuria. Main manifestations: ketonuria Kussmall respirations Fruity acetone smelling breath.

Answer 96

``` More common in Type II, elderly. Fluid deficit is more profound, usually caused by dehydration. Main manifestations: really high glucose levels (>600) small/absent amount of ketones in urine. ```

Answer 97

overnight hypoglycemia, with rebound morning hyperglycemia.

Answer 98

early morning hyperglycemia with no low hypo at night.

Answer 99

- microvascular disease (retinopathies nephropathies and neuropathies) - macrovascular disease (coronary artery, peripheral vascular, and cerebral vascular)

Answer 100

occurs when pts have been exposed to excess cortisol for long periods of time (such as when taking steroids for asthma or arthritis) Patho: no patho is in PP or in book really; it seems lumped together with Cushing Disease

Answer 101

- thinning of scalp hair - acne - facial flush - increased body and facial hair - moon face - supraclavicular fat pad - purple striae - hyperpigmentation - pendulous abdomen - trunk obesity - easy bruising - thin extremities

Answer 102

occurs from overproduction of pituitary ACTH by a pituitary adenoma or by an ectopic secreting nonpituitary tumor ACTH-dependent/ACTH-independent hypercortisolism

Answer 103

results from overproduction of pituitary ACTH by a pituitary adenoma or by ectopic secreting nonpituitary tumor In ACTH- dependent hypercortisolism, the excess ACTH stimulates excess production of cortisol and there is loss of feedback control of ACTH secretion; secretion of both cortisol and adrenal androgens is increased, and cortisol-releasing hormone is inhibited

Answer 104

caused by cortisol secretion from a rare benign or malignant tumor of one or both adrenal glands In ACTH-independent hypercortisolism, the tumors of the adrenal cortex generally only secrete cortisol and tumors secretion of cortisol exceeds normal levels, hypercortisolism occurs

Answer 105

whatever the cause, two observations consistently apply to individuals with hypercortisolism, (1) the normal diurnal or circadian secretion patterns of ACTH and cortisol are lost, and (2) there is no increase in ACTH and cortisol secretion in response to stressor.

Answer 106

Excessive secretion aldosterone by adrenal medulla. Primary: normally from adrenal adenoma (33% of pts. with resistant hypertension) Secondary : by secondary cause such as extra-adrenal stimuli of aldosterone secretion most often angiotensin II through a renin-dependent mechanism. (decreased circulating blood volume

Answer 107

Hyperaldosteronism promotes increased renal sodium and water reabsorption with corresponding hypervolemia and hypertension and renal excretion of potassium

Answer 108

- Hypertension - increased renal sodium and water reabsorption with corresponding hypervolemia - Extracellular fluid overload Edema normally does not occur with primary. -Hypokalemia and hypertension are hallmarks of primary.

Answer 109

Hypocortisolism = Addison Disease Hypocortisolism- low levels of cortisol secretion due to (either/or): - inadequate stimulation of the adrenal glands by ACT -primary inability of the adrenals to produce and secrete cortisol (and other adrenocortical hormones)

Answer 110

Addison Disease is a primary adrenal insufficiency. There is an indadequate synthesis of corticosteroids and mineralocorticoids, with elevated levels of ACTH. It is caused by autoimmune mechanisms that destroys adrenal cortical cells.

Answer 111

* *HYPOTENSION- this is the greatest concern because it can lead to shock. - weakness - easy fatigability - Hyperpigmentation - vitilgo (loss of pigmentation) - Anorexia - Nausea & Vomiting - Diarrhea

Answer 112

Tumor on adrenal gland Patho: sympathetic paraganliomas of the adrenal medula which secrete catecholamines on a continual basis. 10% may be MALIGNANT PRONE TO RUPTURE-NEEDS TO BE REMOVED OR CAN BLEED OUT

Answer 113

``` Hypertension Headache pallor diaphoresis tachycardia palpitations glucose intolerance ```