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*Patho > Weak Points > Flashcards

Weak Points Flashcards

1
Q

Where do hemorrhagic strokes tend to occur?

A

basal ganglia, hypothalamus

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2
Q

Risk factors for aneurysm.

A

HTN, acute alcohol intoxication, cocaine/drug use, congenital defect in medial layer

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3
Q

S/S of aneurysm rupture.

A

severe h/a, photophobia, stiff neck, n/v (meningismus)

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4
Q

S/S of AVM.

A

seizure, neuro changes

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5
Q

Treatment for AVM.

A

XRT, SRS, gamma, glue embol

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6
Q

Patho of meningitis

A
  1. bacterial infection via nasopharynx to CSF
    - bacterial toxins > neuronal apoptosis > alters BBB permeability > edema/inc ICP > dec CPP > hypoxia > necrosis
  2. neutrophils degranulate infected AND healthy tissue (destroyed)
  3. vasculitis > clotting > cerebral infarct
  4. accumulated exudate > obstr hydrocephalus
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7
Q

Affected part of brain for ALZ dz.

A

frontal, temporal lobes

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8
Q

Affected part of brain for Parkinson’s

A

substantia nigra (basal ganglia)

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9
Q

Patho of delrium

A
  • hyperactivity of ANS - hyperkinetic confusional state
  • PSNS - confusion/hypokinetic
  • SNS - agitated/excoted syndrome
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10
Q

Characteristics of of VCI dementia

A
  1. r/t cerebrovascular pathology (white m lesion, microinfarct, ATH, b carotid stenosis
  2. white matter
  3. damage > large cerebral infarct
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11
Q

Patho of VCI dementia

A 
1. endothelial injury causes:
Hypoixa
Inflammation
Oxidative stress
all leading to apoptosis (neurodegeneration)
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12
Q

Patho of parkinson’s

A
  • motor impairment; degeneration of DOPA neurons; residule DOPA n = lewy bodies
  • mechanisms > cell death:
    1. Free radicals
    2. mitochondrial dysfunction
    3. influx Ca++
    4. Neurotrophic factors
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13
Q

TRx for parkinson’s

A

no cure

inc DOPA - dopa precursors, dopa agonists, MAOIs, anticholinergics

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14
Q

Patho of MS

A
  • autoimmune demyelinating dz of CNS; often optic/oculomotor n and spinal tract
  • pattern 3 and 4 = injured ODG = no remyelination
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15
Q

Patho of ALS

A
  • hardening of upper/lower MOTOR neurons
  • unknown cause
  • mechanisms: NOME
    1. neuroinflammation
    2. oxidative stress
    3. mitochondrial dysfxn
    4. excitotoxicity
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16
Q

spinal shock

A

-immediate temp loss of reflexes below injury

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17
Q

neurogenic shock

A

-cervical/upper thoracic injury
-loss of SNS control:
hypotension, brady, CV collapse, high injury can impair resp muscles

18
Q

autonomic dysreflexia (what is it)

A
  • result of neurogenic shock; injury at T6 or above
  • hyperreflexive response to SNS below injury
  • HTN, h/a, brady, flushing above injury, clammy below
19
Q

pathos of autonomic dysreflexia

A

-stimulus (visceral) triggers SNS > vasoconstriction (significant in splanchnic) > inc perihph resist > inc BP
followed by:
-PSNS to lower BP (PSNS + lack of SNS tone) > periph vasodilation > hypotension (pooling)

20
Q

GBS patho
symptoms
trx

A
  • demyelination of PNS mediated by T and B cells
  • ascending weakness or paralysis (can affect resp)
  • support, plasmapheresis, Ig
21
Q

arterial thrombus characteristics:

A
  • begin at site of injury/turbulence
  • grow retrograde
  • MI - wall (mural) clot
  • r/t ATH
22
Q

characteristics of venous thrombus

A
  • r/t stasis
  • prone to embolize
  • antergrad growth
  • large area of attachment/occlusive
23
Q

systemic thromboembolism

A
  • starts intracardiac (LV wall, dilated LA)
  • goes to LE, brain, GI, kidneys, spleen
  • r/t ulcerated plaque or AA
24
Q

characteristics of pulmonary thromboembolism

A
  • originates as DVT to lungs
  • usually multiple
  • clinically silent
  • > 60% pulm circ occluded = death, CV collapse, CP
25
Q

DIC

A
  • widespread of clots (active thrombin > antithrombin = spreads)
  • 2nd complication i.e. sepsis, placenta, cancer = homeo imbalance
  • TF released (thrombin, clotting cascade)
  • fibrin clot formed (fibrin)
  • fibrinolysis (plasmin, breakdown)
  • dim fibrinolysis
  • RESULT: consumption/dec of PL and clotting factor; inc FDP and D-dimer
  • followed by hemorrhage
26
Q

indicates + Dx of mono

A

> 50% lymphocytes; 10% atypical lymphocytes (activated)

27
Q

features of mono

A
  • linked to EBV
  • lymphocyte receptor binds to EBV (antigen)
  • resemble mono: CMV, hepatitis, flu, HIV
  • symptoms: f, s/t, swollen c nodes, inc lymph, atypical lymph
28
Q

what genetic abnormality is hallmark for leukemias?

A

translocation of chrom 9 and 22 (philadelphia chrom)

29
Q

+ Dx of ALL

A

->30% lymphoBLASTS

30
Q

feature of AML

A

-affects myeloid precursors

31
Q

features of CML

A
  • chrom 22 (philadelphia)
  • polycythemia vera is precursor
  • affects myeloid stem cells but presents when mature
32
Q

features of CLL

A

-B lymphocytes cannot convert into plasma cells (no fxn)

33
Q

features of NHL

A
  • cloned B, T, NK cells
  • involve mutated proto-oncogenes and TSG
  • linked to chrom translocations, infections, environment, immunidef, autoimmune
34
Q

features of Burkitt’s

A
  • affects B lymphocytes
  • mutated MYC d/t translocation to chrom 14 (also close to IgG) = stimulate overexpression of growth genes
  • Trx: chemo targeted at disrupting DNA and cell growth
35
Q

features of poly. vera and treatment

A
  • inc in all blood cells (splenomegaly)
  • inc sensitivity to GF
  • 4 stages; myelofibrosis and acute leukemia
  • hypervolemia
  • trx: phlebotomy
36
Q

anemia of chronic dz

A
  • dec erythrocyte life span
  • dec BM response to erythropoeisis (chronic weakened immunity)
  • altered iron metabolism
37
Q

features and types of anaplastic anemia

treatment

A
  • PANcytopenia = dec cells in BM with inc fat
  • PRCA = type of AA
  • faconi’s anemia = precursor to AA
  • TRX: BM/peripheral stem cell trx, immunologic
  • cause: autoimmune vs stem cell
38
Q

How do you Dx hemolytic anemia and where does it occur?

A
  • Dx: lab tests, BM studies, + inc ERY precursors in BM and in circulation
  • occur intravascularly and extra (lymphoid tissues)
39
Q

which anemias have hgb synthesis problems vs RBC destruction?

A

hgb synthesis: all anemias except…

destruction: hemolytic, thalassemia, anemias of chronic dz

40
Q

translocation

A

crossing over of NON-homologous chroms

41
Q

nondisjunction

A
  • chromatids fail to separate properly
  • occurs in meiosis I or II
  • contributes to aneuploidy (trisomy/monosomy gene d/o)
42
Q

crossingover

A
  • rearrangment of homologous chroms

- occurs in prophas I (before nondisjunction can occur)

*Patho (6 decks)

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