Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

Patho > Endocrine/neuro/inflammation > Flashcards

Endocrine/neuro/inflammation Flashcards

(87 cards)

Start Studying
1
Q

Mineralcorticoids

A

Salt-water hormones

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Androgens

A

Male hormones

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Aldosterone

A

Controlled by angiotensin which is controlled by renin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Congenital adrenal hyperplasia

A

Enzymatic defects in the biosynthesis of cortisol from cholesterol

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

21-hydroxylase deficiency

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Simple virilizing CAH

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Salt wasting CAH signs and symptoms

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

11 beta hydroxylase deficiency

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Addison’s signs/symptoms

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Acute adrenal insufficiency

A

Sudden loss of adrenal cortical function, life threatening

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Waterhouse-friderichsen syndrome

A

Acute, bilateral, hemorrhagic infarction of the adrenal cortex

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Cushing’s syndrome

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Conn syndrome

A

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

Hypertension, hypokalemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Pheochromocytoma

A

Neoplasm composed of chromatic cells, synthesize and release catecholamines

Surgically correctable forms of hypertension, rule of 10’s

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Neuroblastoma

A

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

Sporadic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Glucocorticoids

A

Sugar hormones

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

SLE epidemiology

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
SLE clinical features
Butterfly rash, discoid appearance (hands), non erosive joint involvement, hematuria/proteinuria, arteritis, hemolysis, thrombocytopenia
26
Sjorgen epidemiology
4-11 per 100,000 incidence F>M 9:1 >40 years old Related to SLE or RA
27
Sjorgen pathophysiology
Autoimmunity to epithelial salivary cells Inflammation of exocrine glands Dryness of eyes and mouth
28
Sjorgen pathology
Lymphocytic infiltration of epithelial tissue of salivary and lacrimal glands
29
Sjorgen clinical features
Xerostomia, xerophthalmia Severe: hypothyroid, lymphoma, grave's, peripheral neuropathy
30
Inflammatory myositis epidemiology
RARE 5 in 1 million F>M 2:1 Bimodal peak of childhood and 40-50
31
Inflammatory myositis pathophysiology
Patchy involvement | Inflammatory infiltrates of striated muscle
32
Polymyositis pathophysiology
Inflammation in individual muscle fibers | T cells and macrophages
33
Dermatomyositis pathophysiology
Atrophy of muscle bundles | B cell and CD4+ T cells in perifasicular space
34
Inflammatory myositis clinical features
``` Weakness of proximal limbs Routine tasks are difficult Elevated CPK Changes in EMG Infiltrates found in muscle biopsy Skin: dermatomyositis ```
35
Rheumatoid arthritis epidemiology
``` 1% prevelance 40 per 100,000 incidence 5% in native Americans F>M 3:1 Smoking increases risk ```
36
Rheumatoid arthritis pathogenesis
Genetics/environment cause synovial tissue damage Chronic activation of innate immunity (T cells)
37
Rheumatoid arthritis clinical features
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
Oligodendrocytes
CNS, myelin action
39
Schwann cell
PNS, myelination
40
Corticalbulbar tract
Voluntarily carry info from motor cortex to cranial nerves in brain stem Movement in muscles of the head, fascial expression
41
Corticospinal tract
Voluntarily carry info from the motor cortex to skeletal lower motor neuron Crossover in the medulla Anterior and lateral
42
Extrapyrimidal tract
Carry info from brain stem to involuntary part of motor horn Extra pyramidal symptoms
43
UMN lesion
Problem with pyramidal tracts, no motor output Spastic paralysis, hyperrelfexia, + babinski's sign, clonus, clasped knife reflex
44
LMN lesion
Flaccid paralysis, significant atrophy, fasciculations/fibrillations present, hyporeflexia
45
Spinocerebellar tract
Start in spinal cord, end in cerebellum, conveys info about length and tension of muscle fibers (proprioceptive sensation)
46
Spinothalamic tract
Sensory pathway, skin to thalamus Anterior- crude touch Lateral- pain and temperature **cross over at entry level of spine
47
Epidural hematoma pathogenesis
Head trauma, accidents, falls, assaults, skull fractures Blood vessel breaks open in epidural space
48
Epidural hematoma clinical features
Lens shaped appearance, headache, mental status change, vomiting, drowsiness/confusion, aphasia, seizures
49
Parkinson's epidemiology
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
Parkinson's pathology
Lewy bodies in substantia nigra
51
Parkinson's pathogenesis
Inhibition of ATP production of mitochondrial cells in dopaminergic neurons in substantia nigra
52
Parkinson's clinical features
Bradykinesia, rest tremor, rigidity, postural instability
53
ALS epidemiology
1-3 per 100,000 M>F 20-70 years old, incidence increases with each decade Genetic predisposition
54
ALS pathogenesis
Not totally know | Degenerative disease of brain and spinal cord
55
ALS pathology
Degeneration of motor neurons in primary motor cortex and anterolateral horns of spinal cord Muscle atrophy Gliosis in neurons of corticospinal/corticobulbar tracts
56
ALS clinical features
``` **in tact sensation** Asymmetric limb weakness Dysarthria/dysphagia Neck/torso/back weakness Behavioral changes SOB/fatigue Dementia ```
57
Huntington's pathogenesis
Huntington protein produces death in striatum and caudate | Decrease of GABA output
58
Huntington's pathology
Atrophy of basal ganglia | Neuronal loss in striatum and caudate
59
Huntington's clinical features
Chorea Dementia Psychiatric problems
60
Friedreich ataxia pathogenesis
Mitochondrial accumulation of iron | Frataxin moves metal into cells
61
FA pathology
Atrophy of spinal cord and medulla Enlarged heart Accumulation of iron in mitochondria
62
FA clinical features
``` Cerebellum dysfunction Cannot coordinate arm/body position Mistaken for being intoxicated SOB/fatigue (cardiomyopathy) Glucose intolerance (DM, effects pancreas) ```
63
Alzheimer's epidemiology
6.5% prevelance in >65 years of age Incidence doubles every 10 years after the age of 60 Family history APOE e4 allele
64
Alzheimer's pathogenesis
Overproduction/decreased clearance of amyloid beta peptides | Intra neuronal neurofibrillary tangles
65
Alzheimer's pathology
Extra cellular amyloid beta deposition | Neurofibrillary tangles inside the neurons
66
Alzheimer's clinical features
``` Memory impairment Decrease in executive function/problem solving Behavioral/psychological symptoms Apraxia (can't coordinate motor events) Olfactory dysfunction ```
67
Myasthenia gravis pathogenesis
Neuromuscular toxins inhibit ACh | Antibodies attack ACh receptors
68
MG pathology
Antibodies in synaptic cleft on ACh receptors | Lowered ACh in synaptic cleft
69
MG clinical features
Weakness with repetitive movements Ptosis (drooping of the eyelid) Fluctuating weakness in ocular, bulbar, limb, and respiratory muscles
70
Dementia pathogenesis large artery stroke
Cortical areas of the brain
71
Dementia pathogenesis small artery stroke
Sub cortical areas of the brain (basal ganglia, cerebellum, brain stem)
72
Dementia pathogenesis chronic sub cortical ischemia
Lacunar infarct PLUS white matter changes
73
Dementia pathology
Alzheimer's, associated with movement disorders, ALS, vascular causes, inflammatory causes
74
Dementia clinical features (general)
``` 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
Dementia clinical features cortical stroke
Hemiparesis, agnosia, visuospatial difficulty, abrupt onset and stepwise deterioration
76
Dementia clinical features sub cortical stroke
Personality/mood changes, abulia, apathy, depression, gait disturbance, poor balance Gradual OR stepwise Slow OR abrupt onset
77
Seizure pathogenesis
Mass, tumor, infections, metabolic, infarct (stroke) Neuro plasticity Genetic predisposition
78
Epilepsy pathology
Scarring of hippocampal areas Glial dysfunction with uptake of glutamate and potassium Cortical malformations
79
Focal seizures Patho
One or more localized foci, may propagate to right or left hemisphere Result of one or more CNS insults More common in adults
80
Focal seizures clinical features
``` Aura Motor- elementary or complex Dyscognitive- altered awareness/responsiveness Autonomic- GI, cardiac, thermoregulatory Consciousness/awareness/memory preserved ```
81
Generalized seizures Patho
Both hemispheres Genetic predisposition Usually children
82
Absence seizures
Abrupt onset and offset of altered awareness
83
Tonic-clonic (grand mal) seizures
Convulsive, usually bilateral and variations of symmetric, head and eye deviation
84
Clonic seizures
Series of rhythmic jerks
85
Tonic seizures
Bilateral increased tone of limbs for seconds to minutes
86
Atonic seizures
Sudden loss of control of muscles, usually legs
87
Myoclonic seizures
Muscle contractions lasting a fraction of a second

Patho (5 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions