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Final Flashcards

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1
Q

Path of Graves

A

Hyperthyroidism

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2
Q

Risks of hyper parathyroid

A

High risk of path fractures

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3
Q

Effects of Aging on the Endocrine System

A

Altered biologic activity of hormones.
Altered circulating levels of hormones.
Altered secretory responses of endocrine glands.
Altered metabolism of hormones.
Loss of circadian control of hormone release
Changes in secretion of hypothalamic regulatory hormones.
Atrophy of the thyroid gland and diminished secretion of thyroid hormones.
Pancreatic fat deposition, decrease in insulin secretion and in insulin sensitivity.

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4
Q

Goal Of DM Treatment

A

Goal of treatment is to prevent complications.

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5
Q

HgbA1C Levels

A

Normal: 4% - 5.6%
Increased risk for diabetes: 5.7% - 6.4%
Diagnosis of diabetes: 6.5% or higher

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6
Q

Diagnosis Gestational Diabetes

A

Initial glucose challenge test: Blood test done one hour after drinking a glucose solution.

Normal: <130 – 140 mg/dL, or 7.2 – 7.8 mmol/L

Follow-up glucose tolerance testing: Ingest a higher concentration glucose solution after fasting overnight.

Blood glucose gets measured every hour for 3 hours. Diagnosis of gestational diabetes based on at least 2 of the readings being elevated

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7
Q

Clinical Symptoms of Diabetic ketoacidosis (DKA):

A 
Polyuria &amp; dehydration.
Kussmaul respirations (deep, labored breathing pattern).
Sweet or “fruity” breath odor.
Nausea &amp; vomiting.
Abdominal pain. 
Weakness/fatigue.
Lethargy, confusion.
Hyperglycemia.
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8
Q

Clinical Symptoms Hyperosmolar Hyperglycemic Nonketotic Syndrome (HHNS):

A 
Dehydration, polyuria, polydipsia,
Warm dry skin that does not sweat.
Fever (over 101 degrees Fahrenheit).
Lethargy/confusion.
Loss of vision, hallucinations, 
Weakness.

Labs: Serum glucose > 600, absent or low urine ketones.

Delayed sexual maturation (adolescents).

Immunosuppression leading to increased risk of infection and impaired wound healing

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9
Q

Hyperosmolar Hyperglycemic Nonketotic Syndrome (HHNS): Most common in?

A

More common in type 2 diabetes.

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10
Q

Diabetic ketoacidosis (DKA): Most common in?

A

More common in type 1 diabetes.

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11
Q

Clinical Symptoms Hypoglycemia

A

Altered mental status
Tachycardia.
Hypotension
Pale, cool, clammy skin; coma.

In neonates onset may be a few hours to 1 week after birth:

Jitteriness; convulsions; episodic cyanosis; apnea or tachycardia; lethargy & poor feeding; high-pitched cry; diaphoresis; pallor; hypothermia

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12
Q

Criteria for diagnosing rheumatoid arthritis (4 or more)

A 
Evaluation (four or more of the following)
Morning joint stiffness lasting at least 1 hour
Arthritis of three or more joint areas
Arthritis of the hand joints
Symmetric arthritis
Rheumatoid nodules
Abnormal amounts of serum RF
Radiographic changes
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13
Q

Test for Carpal Tunnel

A

Tinel’s sign: Positive if symptoms are reproduced by tapping median nerve at the wrist

Carpal compression test: Positive if numbness & tingling develop with direct pressure over carpal tunnel

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14
Q

Pathophysiology of carpal tunnel syndrome

A

Entrapment neuropathy of median nerve at the wrist.

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15
Q

How to test for scoliosis

A

Adam’s Forward Bend Test —(Most Common and easiest to perform) With feet and knees together, ask the child to bend forward with their arms dangling. The nurse will stand first behind the child and then in front of child to check for any visible curvature, or any uneven appearance in your ribcage, hipbones, or shoulder blades.

Scoliometer —This device is used to measure the actual degree of curvature of the child’s spine. Ask the child to stand with feet and knees together, and bend forward until you, the examiner can see curvature in the child’s upper spine. The inclinometer is then placed on the child’s back, and a measurement is taken.

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16
Q

Bone density levels for diagnosing osteoporosis

A

Normal bone - 833 mg/cm2

Osteopenic bone - 833 to 648 mg/cm2

Osteoporosis - <648 mg/cm2

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17
Q

Which cranial nerve is affected in trigeminal neuralgia

A

Caused by compression of the 5th cranial nerve root usually by vascular structure or malformation

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18
Q

Differentiate types of cerebral palsy

A 
Spastic - Tense contraed ( Most common).
Athetoid - Constant uncontrolled motion of limbs head eyes. 
Rigidity - tight muscles that resist.
Tremor - uncontrollable shaking.
Ataxic - Poor semi of balance.
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19
Q

Pathophysiologic changes seen in Alzheimer’s disease

A

Progresses from mild short-term memory deficits and culminates in a total loss of cognition and executive functions; exhibits different stages.
Includes forgetfulness; emotional upset; disorientation; confusion; lack of concentration; and declines in abstraction, problem solving, and judgment.
Has an insidious onset.

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20
Q

Clinical manifestations of Bell’s palsy

A

Usually due to inflammation of the 7th cranial nerve.
Most patients have sudden onset of a unilateral facial droop, accompanied by drooling (especially in young children) and failure to completely close the affected eye

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21
Q

Area of brain affected by Parkinson’s disease

A

Severe degeneration of the basal ganglia (corpus striatum) involving the dopaminergic nigrostriatal pathway

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22
Q

Parkinson’s disease Neurotransmitter

A

Dopamine deficiency

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23
Q

Clinical Manifestations of Parkinson’s disease:

A

Wide-eyed, unblinking, staring expression with immobile facial muscles
Frequent drooling
Slow gait
Short, shuffling steps
Flexed and abducted arms held stiffly at the side
Slightly forward bending trunk

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24
Q

Causes of vertigo

A

Peripheral vestibular dysfunction:
Benign positional vertigo: debris in semicircular canal.
Occurs with change in position with a delay between movement & symptoms.
Inner ear infection
Meniere’s disease: Swelling of the endolymphatic system

25
Q

Differentiate types of seizures

A

Generalized seizures: Neurons bilaterally
Partial (focal) seizures: Neurons unilaterally
Secondary generalization: Partial moves to generalized
Status epilepticus - Is a medical emergency. (5min - 30)

26
Q

Most common form of epilepsy in children

A

Rolandic Epilepsy of Childhood

27
Q

Symptoms of post-concussive syndrome

A 
Headache
Nervousness or anxiety
Irritability
Insomnia
Depression
Inability to concentrate, forgetfulness
Fatigability
28
Q

3 Stages of Lyme disease and clinical manifestations associated with each stage

A

1 (acute localized): Within 1 month of bite, a bull’s eye rash with flulike symptoms

2 (systemic infection): Cardiac and neurologic manifestations

3 (chronic stage): Arthritis with paraesthesias, radiculopathy, cognitive deficits, memory loss

29
Q

Pathophysiology of gout

A

Is a metabolic disorder that disrupts the body’s control of uric acid production or excretion.
Exhibits high levels of uric acid in the blood and other body fluids.
Occurs when the uric acid concentration increases to high enough levels to crystallize.
Crystals deposit in connective tissues throughout the body.
If prolonged in joints: Gouty arthritis
Tophi: Small, white visible nodules

30
Q

Acute gouty arthritis clinical manifestations

A

A single peripheral joint is almost always involved in all initial episodes. Typically local irritation and aching proceeds to tissues becoming swollen, red, hot, shiny and extremely painful. The pain is often describes as the worst ever experienced. By 24 hours inflammation is maximal, and it then resolves slowly over a week or so, often with itching and flaking of overlying skin.
Increase in serum urate concentration: Hyperuricemia

31
Q

Physiologic changes caused by osteoarthritis

A

Common age-related disorder of synovial joints
Inflammatory joint disease
Loss of articular cartilage, sclerosis of underlying bone, and formation of bone spurs (osteophytes)

32
Q

Tension-type headache

A

Most common
Mild-to-moderate bilateral headache with a sensation of a tight band or pressure around the head
Acute and chronic forms

33
Q

Cluster headache

A

Several attacks occurring during the day for days, followed by a long period of spontaneous remission
Trigger factors
Activation of the trigeminal system
Two forms: Acute and chronic
Clinical manifestations
Pain: Unilateral, intense, tearing, and burning
Sympathetic nervous system underactivity and parasympathetic overactivity

34
Q

Migraine headache

A

Lasts 4 to 72 hours.
Trigger factors; may or may not have an aura.
Most common in women between ages 30-45
Occur in 3%-5% of children before puberty; increases to 10%-20% during 2nd decade of life
Risk factors: Stress, alcohol, caffeine, menstruation, chocolate, caffeine/nicotine withdrawal, too much or too little sleep; missing meals.

When any two symptoms occur: Unilateral head pain, pulsating pain, pain worsening with activity, moderate or severe pain
One of the following symptoms: Nausea or vomiting, or both, photophobia, phonophobia

35
Q

Pathophysiology of multiple sclerosis

A

Progressive, chronic, inflammatory, demyelinating, autoimmune disorder of the CNS
Occurs in white and gray matter
Degeneration of the myelin sheath in CNS neurons, scarring, and loss of axons
Most affected: Women

36
Q

Pathophysiology of amyotrophic lateral sclerosis

A

Lou Gehrig disease.
Is a degenerative disorder diffusely involving the lower and upper motor neurons.

Progressive muscle weakness leads to respiratory failure and death usually 2 to 5 years from symptom onset.
Lower motor neuron syndrome of flaccid paresis consists of a weakness of individual muscles, progressing to paralysis, hypotonia, and primary muscle atrophy (atrophy caused by denervation).
Upper motor neuron syndrome of spastic paresis consists of a weakness of movement patterns, progressing to paralysis.

37
Q

Risks for developing osteomyelitis

A

Is usually caused by a staphylococcal infection.
Is often outside the body (exogenous); can be from a bloodborne (endogenous) infection.

Diseases that impair blood circulation include: Poorly controlled diabetes. Peripheral arterial disease, often related to smoking. Sickle cell disease.

38
Q

Stages of Lyme Disease (3)

A

1 -(acute localized): Within 1 month of bite, a bull’s eye rash with flulike symptoms

2 - (systemic infection): Cardiac and neurologic manifestations

3 - (chronic stage): Arthritis with paraesthesias, radiculopathy, cognitive deficits, memory loss

39
Q

Function of the parathyroid hormone

A

Produce parathyroid hormone (PTH)
Regulates serum calcium.
Increases serum calcium concentration.
Decreases serum phosphate level.
Serves as co-factor with vitamin D to increase calcium absorption.
Is an antagonist of calcitonin (helps regulate calcium & involved with bone building).
Parathyroid hormone–related peptide (PTHrP)
Has properties similar to PTH.
Plays a role in placental calcium transport, lactation, and fetal tooth development

40
Q

Dawn Phenomenon (Diabetes Complication)

A

Early morning rise in glucose levels caused by nocturnal decrease in insulin and elevation of glucagon.

41
Q

Somogyi Effect (Diabetes Complication)

A

Combination of hypoglycemia with rebound hyperglycemia caused by the effects of counter-regulatory hormones. Most common in in type 1 diabetes and in children.

42
Q

Macrovascular Diabetes Complications 1

A

Associated with hyperglycemia, hyperlipidemia, inflammation, and altered endothelial function. Due to atherosclerosis.

Coronary artery disease: Results from accelerated atherosclerosis, hypertension and increased risk for thrombus formation.

43
Q

Macrovascular Diabetes Complications 2

A

Associated with hyperglycemia, hyperlipidemia, inflammation, and altered endothelial function. Due to atherosclerosis.

Increased risk for stroke & myocardial infarction (“silent” or asymptomatic MI)

Peripheral vascular disease: Consequence of neuropathy and occlusion of large and small arteries with an increased risk of ischemia, necrosis, and amputation

44
Q

Diabetes: Micro- and Macrovascular Complications

Diabetic retinopathy

A

responsible for ~10,000 new cases of blindness each year. Mechanisms include microvascular changes & thrombosis that lead to microvascular occlusion, retinal ischemia, increased vascular permeability, microaneurysm formation, hemorrhages, and neovascularization (formation of functional microvascular networks with red blood cell perfusion) resulting in loss of vision.

45
Q

Diabetes: Micro- and Macrovascular Complications

Diabetic nephropathy

A

Leading cause of renal failure in the U.S. Mechanisms include hyperglycemia, hyperperfusion, oxidative stress, and inflammation with glomerular enlargement & glomerular basement membrane thickening, diffuse intercapillary glomerulosclerosis, and expansion of the mesangial matrix resulting in progressive renal failure.

Caused by vascular and metabolic mechanisms or by a combination of both, with axonal and Schwann cell degeneration, abnormalities in sensory and motor nerve conduction velocity, and involvement of the autonomic nervous system.

46
Q

Hyperosmolar Hyperglycemic Nonketotic Syndrome (HHNS): (Diabetes Complication)

A

Relative or absolute reduction in effective circulating insulin with a concomitant elevation of counter-regulatory hormone. More common in type 2 diabetes.

Symptoms: Dehydration, polyuria, polydipsia, warm dry skin that does not sweat, fever (over 101 degrees Fahrenheit), lethargy/confusion, loss of vision, hallucinations, weakness.

Labs: Serum glucose > 600, absent or low urine ketones.

Delayed sexual maturation (adolescents).
Immunosuppression leading to increased risk of infection and impaired wound healing

47
Q 
Diabetic ketoacidosis (DKA): 
(Diabetes Complication)
A

Develops when there is an absolute or relative deficiency of insulin and an increase in the amounts of insulin counter-regulatory hormones of catecholamines, cortisol, glucagon, and GH, increased lipolysis, and accelerated gluconeogenesis and ketogenesis.

More common in type 1 diabetes.

Symptoms: Polyuria & dehydration, Kussmaul respirations (deep, labored breathing pattern); sweet or “fruity” breath odor; nausea & vomiting, abdominal pain, weakness/fatigue, lethargy, confusion, hyperglycemia. Labs: serum glucose level >250 mg/dL; serum pH < 7.30; urine (+) for ketones, total body (not serum) potassium depletion.

48
Q

Pathophysiology of type 2 diabetes

A

Characterized by a relative insufficiency of insulin due to resistance to the action of insulin in target tissues, decrease in insulin receptors, and/or impairment of insulin secretion.

Etiology & Incidence:
Heterogenous disorder with familial pattern.
Influenced by environmental factors, lack of physical activity, diet high in refined carbohydrate and fat, with low fiber.

No human leukocyte antigen or islet cell antibodies.

Syndrome of hyperinsulinemia and insulin resistance resulting in hyperglycemia, hypertension, and hyperlipidemia.

Type 2 accounts for 90% of all diabetes cases in the U.S.
29.1 million Americans (9.3% of the population)
Children account for 20% of all newly diagnosed cases

49
Q

Clinical manifestations of Cushing disease

A 
Thinning scalp hair
Facial Flush
Acne Increased Body &amp; facial hair
Moon face
Purple striae
Pendulous abd
Easy Bruising 
Subclavicular fat
Truck obesity 
Thin extremities 
Hyper pigmentation
50
Q

Causes of hypothyroidism

A

Deficient production of thyroid hormone by the thyroid gland.

51
Q

Hypothyroidism Adults

A

Anorexia, dry skin, coarse dry hair, alopecia, receding hairline, constipation, cold intolerance, lethargy, increase in weight, irregular/heavy menses, memory loss, depression, muscle aches, myxedema (nonpitting, boggy edema, especially around the eyes, hands, and feet; thickening of the tongue).

Myxedema coma: Medical emergency, diminished level of consciousness; hypothermia without shivering,

hypoventilation, hypotension, hypoglycemia, lactic acidosis, and coma

52
Q

Hypothyroidism Neonates:

A

Persistent jaundice, constipation, poor feeding, lethargy/somnolence, prolonged gestation, increased birthweight.

53
Q

Hypothyroidism Children

A

Children: Family history, poor growth, learning disability, fatigue, constipation, weight gain, cold intolerance.

54
Q

Impact of gestational diabetes on baby

A

Insulin does not cross the placenta but glucose does resulting in high glucose levels in the baby. Causes baby’s pancreas to make extra insulin to get rid of the glucose. Excess energy gets stored as fat – can lead to macrosomia (“fat” baby).

Health risks to the baby include shoulder damage during birth; hypoglycemia at birth; increased risk of breathing problems; risk for childhood obesity and adult onset type 2 diabetes.

55
Q

Symptoms of hypothyroidism

A 
Hypo Function
Loss of hair, brittle hair.
Periorbital edema
Puffy face 
Normal to small thyroid
Bradycardia (HF)
Constipation
Cold intolerance 
Muscle weakness 
Osteoporosis
Edema of extremities
56
Q

Symptoms of hyperthyroidism

A 
Hyper Function
Thin Hair
Exophthalmos 
Normal of enlarged thyroid (warm &amp; nodular)
Tachycardia (HF)
Weight loss
Diarrhea
Warm skin
Hyper reflexia
Pretibial myxedema
57
Q

Lab value diagnostic for adrenal insufficiency

A

Low plasma cortisol <5 mcg/dL in early morning.

The ACTH stimulation test is the most commonly used test for diagnosing adrenal insufficiency

Sodium, chloride, glucose and bicarbonate levels low, with high potassium level.
BUN, plasma renin, ACTH, calcium – all elevated.
CBC – decreased hemoglobin, neutrophils, and eosinophils.
Abdominal CT scan: Small adrenals.
Chest x-ray: Small heart size and adrenal calcification.

58
Q

Functions of insulin

A

Regulated by chemical, hormonal, and neural mechanisms.
Synthesized from proinsulin.
Secretion is promoted by increased blood glucose levels.
Facilitates the rate of glucose uptake into the body’s cells.
Facilitates the intracellular transport of potassium.
Anabolic hormone: Synthesizes proteins, carbohydrates, lipids, and nucleic acids.

59
Q

Functions of Glucagon

A

Insulin antagonist.
Secretion is promoted by decreased blood glucose levels.
Increases glucose by stimulating glycogenolysis (breakdown of glycogen) and gluconeogenesis (generation of glucose from non-carbohydrate carbon substrates such as pyruvate, lactate, glycerol, and glucogenic amino acids..
Stimulates lipolysis.

Nursing 611 Patho (4 decks)

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