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Advanced Pathophysiology > Test 4 Study Guide Questions > Flashcards

Test 4 Study Guide Questions Flashcards

1
Q

What is myasthenia gravis?

A

This is a disorder of the peripheral nervous system and is a chronic autoimmune disorder that affects the neuromuscular junction by causing muscle weakness/fatiguability.

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2
Q

What is the pathogenesis of myasthenia gravis?

A

IgG antibodies attach to the post synaptic acetylcholine receptors that then prevent the attachment of acetylcholine and transmission of nerve impulses. Eventually these receptors will be destroyed.

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3
Q

What are clinical manifestations of myasthenia gravis?

A

Patients will experience diplopia, ptosis, and ocular movement paralysis first. The paralysis will descend and the person will require ventilatory assistance. Over time, the disease will lead to death.

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4
Q

What is meningitis?

A

An infection of the meninges, specifically the pia mater

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5
Q

What are the most common bacterial causes of meningitis?

A

Meningococcus or penumococcus

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6
Q

What are signs and symptoms of meningitis?

A
  1. Photophobia
  2. Kernig’s Sign
  3. Brudzinki’s Sign
  4. Nuchal Rigidity
  5. Seizures
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7
Q

How is meningococcal bacteria transmitted?

A

Meningococcal is transmitted via air droplets and the individual must be isolated for 24 hours after antibiotic therapy is started. Additionally, their contacts should be given prophylactic medications to prevent infection.

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8
Q

What is the most common cause of meningitis in newborns?

A

Group B strep, E.coli, and listeria. Group B strep causes a severe and deadly infection in neonates and is transmitted to the infant from the mother’s birth canal.

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9
Q

What is Parkinson’s disease?

A

It is a degenerative disorder of the basal ganglia (CNS) resulting in the lack of the neurotransmitter, dopamine and is a defect of the substania nigra.

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10
Q

How does basal ganglia impairment affect those with Parkinson’s?

A

The basal ganglia is part of the diencephalon and works with the cerebellum to modify movements, specifically those movements transmitted via the extrapyramidal spinal tracts.

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11
Q

What is the pathogenesis of Parkinson’s disease?

A

The pathogenesis begins with the degeneration of dopamine producing neurons in the basal ganglia. Dopamine deficiency leads to an imbalance of more acetylcholine in the basal ganglia which is responsible for causing the abnormal movements associated with Parkinson’s disease

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12
Q

What are clinical manifestations of Parkinson’s disease?

A
  1. Resting tremor/hypertonia/rigidity
  2. Bradykinesia or akinesia
  3. Abnormal posturing (flexed forward)
  4. Shuffling gait
  5. No facial expression
  6. Weak, slurred speech
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13
Q

What is a subarachnoid hematoma?

A

This is a bleed occurring in the subarachnoid space

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14
Q

What are clinical manifestations of subarachnoid hematoma?

A

Positive Kernig’s and Brudzinski’s signs

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15
Q

What is a complication of subarachnoid hematoma?

A

Cerebral vasospasm (narrowing of brain blood vessel) is a complication of SAH and can lead to cerebral ischemia. can cause interstitial edema which is seen with hydrocephalus

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16
Q

What is Cushing’s Syndrome?

A

This syndrome occurs due to an over secretion of cortisol

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17
Q

What is the purpose of aldosterone and what happens when RAAS is inhibited?

A

The adrenal gland releases mineralocorticoids. The main mineralocorticoid is aldosterone. Aldosterone is the main hormone which regulates sodium in the body. The release of aldosterone is controlled by RAAS and when RAAS is inhibited, this results in a decrease of aldosterone secretion–> potassium accumulation because of increased renal reabsorption of potassium.

When renal sodium is not excreted properly, there is increase in potassium which can lead to arterial HTN in Cushing’s syndrome

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18
Q

What are complications of Cushing’s syndrome (over secretion of cortisol)?

A
  1. Abnormal distribution of fat to areas of body causing truncal obesity, moon afce, and the formation of a buffalo hump.
  2. The breakdown of bone leading to high urine calcium levels and increased risk for renal stones and osteoporosis
  3. Weakened collagen fibers leading to skin fragility and bruising. These patients will have purple striae (stretch marks)
  4. Anti-clotting effects secondary to the inhibition of arachidonic acid pathway which will cause these patients to bleed more easily.
  5. Hyper-secretion of androgens causes hirsutism and acne
  6. increased peripheral vasoconstriction and HTN, secondary to increased sensitivity to
    catecholamines
  7. Increases glucose levels in the body
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19
Q

What is Duchenne muscular dystrophy and how is it caused?

A

This is an x linked genetic disorder and is the most common form of muscular dystrophy. It is caused by the deletion of one or more exons on the DMD gene on the X chromosome.

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20
Q

What is the pathogenesis of DMD?

A

The protein dystrophin is absent in those with Duchenne Muscular Dystrophy, and this lack of dystrophin allows for muscle fibers to be torn apart during contraction. Free calcium then enters the muscle cells and causes cell death/necrosis which increases levels of CK in the body.

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21
Q

What are clinical manifestations of DMD?

A
  1. child will toe walk, have difficulty getting up from floor, and have frequent falls
  2. muscle weakness will start in the pelvic area and will have calf muscle hypertrophy
  3. Kyphoscoliosis, respiratory, and cardiac complications can occur. Most patients will die from pulmonary infections in their mid 20s.
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22
Q

What are the stages of increased intracranial pressure?

A
  1. Brain will compensate for increased ICP by vasoconstriction and compressing the venous system.
  2. ICP continues to increase. By this stage, the brain can no longer compensate for the increased ICP. Patients will start to show symptoms which include confusion, restlessness, lethargy, pupil/breathing changes.
  3. The ICP will approach the brain’s arterial pressure. Cellular hypoxia and hypercapnia begin and the patient decompensates quickly. Intracranial arterial vasodilation occurs secondary to CO2 accumulation. Symptoms include bradycardia, widening pulse pressure, pupils small and sluggish.
  4. Herniation occurs here due to the equalization of the ICP and arterial pressures. This equalization prevents cerebral perfusion causing cell death.
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23
Q

What occurs to the patient in a left sided stroke?

A
  1. Right sided weakness/paralysis
  2. Speech/language problems
  3. Slow, cautious behavior
  4. Impairment of organizational abilities
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24
Q

What occurs to the patient in a right sided stroke?

A
  1. Left sided weakness/paralysis
  2. Vision problems
  3. Quick, overly curious behavior
  4. Poor decision making
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25
Q

What is spinal shock?

A

It is COMPLETE, but TEMPORARY loss of function below the level of injury and occurs immediately post injury.

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26
Q

What are clinical manifestations that occur during spinal shock?

A

Flaccid paralysis of the body including loss of skeletal muscle use, bowel/bladder control, loss of sexual function. These patients will also be unable to regulate body temperature due to hypothalamus dysfunction.

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27
Q

What is an early indicator of diabetic nephropathy?

A

proteinuria and microalbuminuria

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28
Q

What are the 4 types of supratentorial herniations and where do they occur?

A

uncal, central, cingulate, and transcalvarial- these occur above the tentorial membrane

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29
Q

What is an uncal herniation?

A

occurs when a portion of the cerebrum moves through the tentorial notch and compresses the THIRD cranial nerve

30
Q

What are clinical manifestations of uncal herniation?

A
  1. dilated ipsilateral pupils first and then contralateral pupils
  2. decorticate/decerebrate posturing
  3. Cheyne stokes respirations
31
Q

what is a central herniation and what occurs here?

A

central herniation is when the diencephalon is forced down through the tentorial notch. patients will initially have small reactive pupils that later dilate.

32
Q

What occurs in transcalvarial herniation?

A

brain tissue moves through an opening in the skull which may be a result of a skull fracture or a surgical opening.

33
Q

what is an infratentorial herniation?

A

occurs below the tentorial membrane and cerebral tonsillar herniation is the most common type. it is characterized by a downward movement of the cerebellum through the foramen magnum.

34
Q

What are clinical manifestations of cerebral tonsillar herniation?

A

stiff neck, decreased LOC, and respiratory/cardiac abnormalities

35
Q

what is a cluster headache?

A

a severe, stabbing, throbbing headache that is typically unilateral and may alternate sides with each episode. this type of headache occurs in clusters (up to 8/day) and last minutes to hours. they are associated with a tearing eye, nasal drainage, and occur at night which wakes the patient up.

36
Q

what is a tension headache?

A

most common type and is a mild to moderate pain which is felt through the entire head. chronic tension headaches occur at least 15 days a month for 3 months.

37
Q

What is Grave’s disease?

A

Autoimmune disorder which results in over secretion of thyroid hormone (hyperthyroidism).

38
Q

What is the pathogenesis of Grave’s disease?

A

thyroid stimulating antibodies attach to the thyroid cells and mimic the function of TSH which results in increased secretion of T3 and T4.

39
Q

What are clinical manifestations of Grave’s disease?

A
  1. goiter
  2. exophthalmus/periorbital edema, and extra-ocular muscle weakness leading to strabismus and diplopia
40
Q

what are clinical manifestations of hypothyroidism?

A
  1. myxedema (puffy face)
  2. high TSH with low levels of T3 and T4
  3. weight gain/coarse hair/dry skin/ cold intolerance/ low body temp
41
Q

What is a major risk factor to hypothyroidism?

A

iodine deficiency

42
Q

What is the pathogenesis of DM type 2?

A

The basic pathological defect is insulin resistance.

43
Q

what is DKA?

A

acute complication of DM which results from insulin deficiency and the release of counter regulatory hormones. the lack of insulin causes initiation of gluconeogenesis and the formation of ketone bodies and metabolic acidosis.

44
Q

What is Kaussmaul breathing?

A

Kussmaul breathing is an abnormal breathing pattern characterized by rapid, deep breathing at a consistent pace. It’s a sign of a medical emergency — usually diabetes-related ketoacidosis (DKA), which can affect people with diabetes and people with undiagnosed Type 1 diabetes

45
Q

what is the pathogenesis of hyperosmolar hyperglycemic state?

A

HHS occur due to elevated glucose levels which causes high osmotic pressure and osmotic diuresis which leads to severe dehydration, low blood volume, and poor perfusion

46
Q

what is the somogyi effect?

A

the effect happens when a low blood sugar (hypoglycemia) episode overnight leads to high blood sugar (hyperglycemia) in the morning due to a surge of hormones. It can affect people with diabetes who take insulin.

47
Q

What is the pathogenesis of osteoporosis?

A

Bone homeostasis is dependent upon a cytokine receptor activator known as RANKL, its receptor RANK and its decoy receptor osteoprotegerin. Osteoblasts expresses RANKL which is necessary for osteoclast development. The effects of RANKL binding to RANK are controlled by the decoy receptor OPG by allowing RANKL to bind with OPG instead of RANK. An alteration in this system leads to osteoporosis

48
Q

What receptors match with osteoclasts vs osteoblasts?

A

Osteoblasts build up new bone and need RANK ligand

Osteoclasts cut down bone and need RANK for survival

49
Q

What effect does estrogen have on osteoporosis?

A

Estrogen exerts antiapoptotic effects on osteoblasts and proapoptotic effects on osteoclasts

50
Q

What is an increased risk factor for stroke?

A

hypertension

51
Q

What is a Jacksonian march seizure?

A

This is a simple partial seizure which starts with tonic contractions in one hand or on one side of the face which then become more widespread.

52
Q

What is the pathogenesis of alzheimer’s ?

A

It is associated with the apolipoprotein E gene allele 4 on chromosome 19. This disease interferes with amyloid clearance from the brain. The amyloid accumulates in the brain and is transformed into a substance that is toxic to neurons which triggers the formation of plaques and tangles in the brain.

53
Q

What is guillain barre syndrome?

A

autoimmune disease (thought to be B cell/T cell mediated) of the PNS due to a viral infection which then attack the myelin of the PNS and ascending paralysis which starts in the extremities and moves up.

54
Q

How is the hypothalamus associated with Parkinson’s disease?

A

The hypothalamus produces the neurotransmitter dopamine and Parkinson’s disease is caused by a lack of this dopamine.

55
Q

What is receptive dysphagia?

A

This individual is able to produce language but it is not comprehensible; this is a injury to the Wernicke’s area of the temporal lobe

56
Q

What is expressive dysphagia?

A

This individual can understand fully but cannot express through language. this dysphagia affects the Broca’s area of the frontal lobe

56
Q

what does damage to the anterior cerebral artery cause?

A

an occlusion of this artery causes contralateral paralysis and a loss of sensation. the symptoms are more present in the lower extremities rather than in the upper extremities.

57
Q

what does occlusion to the middle cerebral artery cause?

A

occlusion here causes visual changes which will be contralateral to the occlusion

58
Q

what does occlusion in the basilar artery cause?

A

results in quadriplegia, a loss of voluntary facial, mouth, eye, and tongue movements. however, the patients LOC is intact

59
Q

what is a thrombotic stroke?

A

occlusion of the arterial supply to the brain and is usually related to artherosclerosis.

60
Q

what is a embolic stroke?

A

results from fragments of a thrombus from outside the brain. the fragments get logged in and block the arterial blood flow to the brain. this is what commonly happens when people have a stroke from afib.

61
Q

what are risk factors of an embolic stroke?

A

A fib, rheumatic valvular disease, endocarditis, prosthetic valve

62
Q

what is a lacunar stroke?

A

small infarcts of less than 1 cm which occur throughout brain tissue and involves the small arteries

63
Q

what body functions does the hypothalamus regulate?

A

water balance, appetite, vital signs, sleep cycles, pain perception, and links CNS to the endocrine system

64
Q

what does the adrenal medulla secrete?

A

the adrenal medulla secretes the catecholamines epinephrine, norepnephrine, and dopamine

65
Q

what are clinical manifestations of osteoarthritis?

A

joint stiffness that is worse in the morning and is relieved with rest.

66
Q

what is Addison’s disease?

A

this is a disease of the adrenal cortex leading to decreased cortisol and aldosterone secretion

67
Q

what are clinical manifestations of Addison’s disease?

A

Addisonian Triad
1. Hyperkalemia because there is not enough aldosterone to get rid of potassium

  1. hyponatremia not enough aldosterone to retain sodium
  2. hypotension because there is not enough cortisol to maintain vascular tone
68
Q

what is macroangiopathy?

A

chronic complication of diabetes where large blood vessels have fat and blood clots build up and stick to the vessel walls, blocking the flow of blood.

69
Q

what happens pathogenically in macroangiopathy?

A

damage includes thickening of the capillary membrane, endothelial cell hyperplasia, and thrombosis all of which result in decreased perfusion

Advanced Pathophysiology (22 decks)

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