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Patho > Endocrine/neuro/inflammation > Flashcards

Endocrine/neuro/inflammation Flashcards

1
Q

Mineralcorticoids

A

Salt-water hormones

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2
Q

Androgens

A

Male hormones

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3
Q

Aldosterone

A

Controlled by angiotensin which is controlled by renin

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4
Q

Congenital adrenal hyperplasia

A

Enzymatic defects in the biosynthesis of cortisol from cholesterol

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5
Q

21-hydroxylase deficiency

A

Major cause of CAH
chromosome 6 and HLA linked, cytochrome P450 enzyme in ER
Aldosterone and cortisol deficiencies

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6
Q

Simple virilizing CAH

A

Partial 21-hydroxyl are deficiency, but normal cortisol, increased gland size
Increased cortisol precursors, aldosterone, and androgens

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7
Q

Simple virilizing CAH signs and symptoms

A

Females: androgen excess, pubic hair and clitoris enlargement, stunt growth, infertile
Males: no abnormal genitalia at birth, stunt growth, sexual precocity, some infertility but not all

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8
Q

Salt wasting CAH

A

Total or near total deficiency of 21 hydroxyl are enzyme
Hypoaldosteronism develops within the first few weeks of life
Aldosterone production remains low or nonexistent

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9
Q

Salt wasting CAH signs and symptoms

A

Hyponatremia, hyperkalemia, dehydration, hypotension, increased renin secretion, hypoglycemia, increased cortisol precursors, masulinization

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10
Q

Late onset non classic CAH

A

No abnormalities at birth, virilizing symptoms at the time of puberty

Normal cortisol, normal aldosterone, increased 17-hydroxyprogesterone (cortisol precursor), increased androgens/masculinization

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11
Q

11 beta hydroxylase deficiency

A

Chromosome 8, high levels of 11 deoxycortisol (cortisol precursor) causes sodium retention and hypertension

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12
Q

Adrenal cortical insufficiency

A

Deficient production of adrenal cortical hormones

result of: destruction of the adrenal gland, pituitary or hypothalamic dysfunction, intake of corticosteroids

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13
Q

Primary chronic adrenal insufficiency (addison’s)

A

Fatal wasting disorder caused by the failure of the adrenal glands to produce glucocorticoids, Mineralcorticoids, and androgens

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14
Q

Addison’s signs/symptoms

A

Weakness, weight loss, hypotension, low sodium and high potassium levels, tan pigmentation

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15
Q

Acute adrenal insufficiency

A

Sudden loss of adrenal cortical function, life threatening

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16
Q

Waterhouse-friderichsen syndrome

A

Acute, bilateral, hemorrhagic infarction of the adrenal cortex

Hypotension, shock, abdominal/back pain, fever, purpura

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17
Q

Cushing’s syndrome

A

High glucocorticoid levels, causes moon facies, buffalo hump, abdominal striae, hirsutism, etc..

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18
Q

Conn syndrome

A

Hyperaldosteronism, usually adrenal adenoma, 3:1 women, 30-50 years

Hypertension, hypokalemia

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19
Q

Pheochromocytoma

A

Neoplasm composed of chromatic cells, synthesize and release catecholamines

Surgically correctable forms of hypertension, rule of 10’s

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20
Q

Neuroblastoma

A

Extra cranial solid tumors of childhood, first 5 years of life, anywhere in sympathetic nervous system (usually abdomen)

Sporadic

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21
Q

Glucocorticoids

A

Sugar hormones

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22
Q

SLE epidemiology

A

20-150 per 100,000 prevelance
F>M
Asian/AA/African Caribbean/Hispanic American > Caucasian
Older females

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23
Q

SLE pathogenesis

A

Dead cell parts lying around, taken up and activate dendritic and B cells

Antibody formation and inflammation. Flares of SLE show memory

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24
Q

SLE pathology

A

Immune complexes (autoantibodies and auto antigens) deposit into tissues like the kidney

Body tries to clear these deposits which causes damage

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25
Q

SLE clinical features

A

Butterfly rash, discoid appearance (hands), non erosive joint involvement, hematuria/proteinuria, arteritis, hemolysis, thrombocytopenia

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26
Q

Sjorgen epidemiology

A

4-11 per 100,000 incidence
F>M 9:1
>40 years old
Related to SLE or RA

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27
Q

Sjorgen pathophysiology

A

Autoimmunity to epithelial salivary cells
Inflammation of exocrine glands
Dryness of eyes and mouth

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28
Q

Sjorgen pathology

A

Lymphocytic infiltration of epithelial tissue of salivary and lacrimal glands

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29
Q

Sjorgen clinical features

A

Xerostomia, xerophthalmia

Severe: hypothyroid, lymphoma, grave’s, peripheral neuropathy

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30
Q

Inflammatory myositis epidemiology

A

RARE
5 in 1 million
F>M 2:1
Bimodal peak of childhood and 40-50

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31
Q

Inflammatory myositis pathophysiology

A

Patchy involvement

Inflammatory infiltrates of striated muscle

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32
Q

Polymyositis pathophysiology

A

Inflammation in individual muscle fibers

T cells and macrophages

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33
Q

Dermatomyositis pathophysiology

A

Atrophy of muscle bundles

B cell and CD4+ T cells in perifasicular space

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34
Q

Inflammatory myositis clinical features

A 
Weakness of proximal limbs
Routine tasks are difficult
Elevated CPK
Changes in EMG
Infiltrates found in muscle biopsy
Skin: dermatomyositis
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35
Q

Rheumatoid arthritis epidemiology

A 
1% prevelance
40 per 100,000 incidence
5% in native Americans
F>M 3:1
Smoking increases risk
36
Q

Rheumatoid arthritis pathogenesis

A

Genetics/environment cause synovial tissue damage

Chronic activation of innate immunity (T cells)

37
Q

Rheumatoid arthritis clinical features

A

MCP and PIP joints of hands and feet affected first
Wrist, elbow, knee, shoulder, cervical spine then affected
Fever/fatigue = flare
Lung parenchyma, artery inflammation, eyes, pericardium

38
Q

Oligodendrocytes

A

CNS, myelin action

39
Q

Schwann cell

A

PNS, myelination

40
Q

Corticalbulbar tract

A

Voluntarily carry info from motor cortex to cranial nerves in brain stem

Movement in muscles of the head, fascial expression

41
Q

Corticospinal tract

A

Voluntarily carry info from the motor cortex to skeletal lower motor neuron

Crossover in the medulla

Anterior and lateral

42
Q

Extrapyrimidal tract

A

Carry info from brain stem to involuntary part of motor horn

Extra pyramidal symptoms

43
Q

UMN lesion

A

Problem with pyramidal tracts, no motor output

Spastic paralysis, hyperrelfexia, + babinski’s sign, clonus, clasped knife reflex

44
Q

LMN lesion

A

Flaccid paralysis, significant atrophy, fasciculations/fibrillations present, hyporeflexia

45
Q

Spinocerebellar tract

A

Start in spinal cord, end in cerebellum, conveys info about length and tension of muscle fibers (proprioceptive sensation)

46
Q

Spinothalamic tract

A

Sensory pathway, skin to thalamus

Anterior- crude touch
Lateral- pain and temperature
**cross over at entry level of spine

47
Q

Epidural hematoma pathogenesis

A

Head trauma, accidents, falls, assaults, skull fractures

Blood vessel breaks open in epidural space

48
Q

Epidural hematoma clinical features

A

Lens shaped appearance, headache, mental status change, vomiting, drowsiness/confusion, aphasia, seizures

49
Q

Parkinson’s epidemiology

A

41 per 100,000 in 40-49 years of age prevelance
1900 per 100,000 in 80 or older years of age prevelance
Screen for pesticide exposure, depression

50
Q

Parkinson’s pathology

A

Lewy bodies in substantia nigra

51
Q

Parkinson’s pathogenesis

A

Inhibition of ATP production of mitochondrial cells in dopaminergic neurons in substantia nigra

52
Q

Parkinson’s clinical features

A

Bradykinesia, rest tremor, rigidity, postural instability

53
Q

ALS epidemiology

A

1-3 per 100,000
M>F
20-70 years old, incidence increases with each decade
Genetic predisposition

54
Q

ALS pathogenesis

A

Not totally know

Degenerative disease of brain and spinal cord

55
Q

ALS pathology

A

Degeneration of motor neurons in primary motor cortex and anterolateral horns of spinal cord

Muscle atrophy
Gliosis in neurons of corticospinal/corticobulbar tracts

56
Q

ALS clinical features

A 
**in tact sensation**
Asymmetric limb weakness
Dysarthria/dysphagia
Neck/torso/back weakness
Behavioral changes
SOB/fatigue
Dementia
57
Q

Huntington’s pathogenesis

A

Huntington protein produces death in striatum and caudate

Decrease of GABA output

58
Q

Huntington’s pathology

A

Atrophy of basal ganglia

Neuronal loss in striatum and caudate

59
Q

Huntington’s clinical features

A

Chorea
Dementia
Psychiatric problems

60
Q

Friedreich ataxia pathogenesis

A

Mitochondrial accumulation of iron

Frataxin moves metal into cells

61
Q

FA pathology

A

Atrophy of spinal cord and medulla
Enlarged heart
Accumulation of iron in mitochondria

62
Q

FA clinical features

A 
Cerebellum dysfunction
Cannot coordinate arm/body position
Mistaken for being intoxicated
SOB/fatigue (cardiomyopathy)
Glucose intolerance (DM, effects pancreas)
63
Q

Alzheimer’s epidemiology

A

6.5% prevelance in >65 years of age
Incidence doubles every 10 years after the age of 60
Family history
APOE e4 allele

64
Q

Alzheimer’s pathogenesis

A

Overproduction/decreased clearance of amyloid beta peptides

Intra neuronal neurofibrillary tangles

65
Q

Alzheimer’s pathology

A

Extra cellular amyloid beta deposition

Neurofibrillary tangles inside the neurons

66
Q

Alzheimer’s clinical features

A 
Memory impairment
Decrease in executive function/problem solving
Behavioral/psychological symptoms
Apraxia (can't coordinate motor events)
Olfactory dysfunction
67
Q

Myasthenia gravis pathogenesis

A

Neuromuscular toxins inhibit ACh

Antibodies attack ACh receptors

68
Q

MG pathology

A

Antibodies in synaptic cleft on ACh receptors

Lowered ACh in synaptic cleft

69
Q

MG clinical features

A

Weakness with repetitive movements
Ptosis (drooping of the eyelid)
Fluctuating weakness in ocular, bulbar, limb, and respiratory muscles

70
Q

Dementia pathogenesis large artery stroke

A

Cortical areas of the brain

71
Q

Dementia pathogenesis small artery stroke

A

Sub cortical areas of the brain (basal ganglia, cerebellum, brain stem)

72
Q

Dementia pathogenesis chronic sub cortical ischemia

A

Lacunar infarct PLUS white matter changes

73
Q

Dementia pathology

A

Alzheimer’s, associated with movement disorders, ALS, vascular causes, inflammatory causes

74
Q

Dementia clinical features (general)

A 
Decline in cognition in 1 or more of the following domains that interferes with daily living:
Learning/memory
Language
Executive function
Complex attention
Perceptual- motor
Social cognition
75
Q

Dementia clinical features cortical stroke

A

Hemiparesis, agnosia, visuospatial difficulty, abrupt onset and stepwise deterioration

76
Q

Dementia clinical features sub cortical stroke

A

Personality/mood changes, abulia, apathy, depression, gait disturbance, poor balance

Gradual OR stepwise
Slow OR abrupt onset

77
Q

Seizure pathogenesis

A

Mass, tumor, infections, metabolic, infarct (stroke)
Neuro plasticity
Genetic predisposition

78
Q

Epilepsy pathology

A

Scarring of hippocampal areas
Glial dysfunction with uptake of glutamate and potassium
Cortical malformations

79
Q

Focal seizures Patho

A

One or more localized foci, may propagate to right or left hemisphere
Result of one or more CNS insults
More common in adults

80
Q

Focal seizures clinical features

A 
Aura
Motor- elementary or complex
Dyscognitive- altered awareness/responsiveness
Autonomic- GI, cardiac, thermoregulatory
Consciousness/awareness/memory preserved
81
Q

Generalized seizures Patho

A

Both hemispheres
Genetic predisposition
Usually children

82
Q

Absence seizures

A

Abrupt onset and offset of altered awareness

83
Q

Tonic-clonic (grand mal) seizures

A

Convulsive, usually bilateral and variations of symmetric, head and eye deviation

84
Q

Clonic seizures

A

Series of rhythmic jerks

85
Q

Tonic seizures

A

Bilateral increased tone of limbs for seconds to minutes

86
Q

Atonic seizures

A

Sudden loss of control of muscles, usually legs

87
Q

Myoclonic seizures

A

Muscle contractions lasting a fraction of a second

Patho (5 decks)

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