Weak Points Flashcards
Where do hemorrhagic strokes tend to occur?
basal ganglia, hypothalamus
Risk factors for aneurysm.
HTN, acute alcohol intoxication, cocaine/drug use, congenital defect in medial layer
S/S of aneurysm rupture.
severe h/a, photophobia, stiff neck, n/v (meningismus)
S/S of AVM.
seizure, neuro changes
Treatment for AVM.
XRT, SRS, gamma, glue embol
Patho of meningitis
- bacterial infection via nasopharynx to CSF
- bacterial toxins > neuronal apoptosis > alters BBB permeability > edema/inc ICP > dec CPP > hypoxia > necrosis - neutrophils degranulate infected AND healthy tissue (destroyed)
- vasculitis > clotting > cerebral infarct
- accumulated exudate > obstr hydrocephalus
Affected part of brain for ALZ dz.
frontal, temporal lobes
Affected part of brain for Parkinson’s
substantia nigra (basal ganglia)
Patho of delrium
- hyperactivity of ANS - hyperkinetic confusional state
- PSNS - confusion/hypokinetic
- SNS - agitated/excoted syndrome
Characteristics of of VCI dementia
- r/t cerebrovascular pathology (white m lesion, microinfarct, ATH, b carotid stenosis
- white matter
- damage > large cerebral infarct
Patho of VCI dementia
1. endothelial injury causes: Hypoixa Inflammation Oxidative stress all leading to apoptosis (neurodegeneration)
Patho of parkinson’s
- 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
TRx for parkinson’s
no cure
inc DOPA - dopa precursors, dopa agonists, MAOIs, anticholinergics
Patho of MS
- autoimmune demyelinating dz of CNS; often optic/oculomotor n and spinal tract
- pattern 3 and 4 = injured ODG = no remyelination
Patho of ALS
- hardening of upper/lower MOTOR neurons
- unknown cause
- mechanisms: NOME
1. neuroinflammation
2. oxidative stress
3. mitochondrial dysfxn
4. excitotoxicity
spinal shock
-immediate temp loss of reflexes below injury
neurogenic shock
-cervical/upper thoracic injury
-loss of SNS control:
hypotension, brady, CV collapse, high injury can impair resp muscles
autonomic dysreflexia (what is it)
- result of neurogenic shock; injury at T6 or above
- hyperreflexive response to SNS below injury
- HTN, h/a, brady, flushing above injury, clammy below
pathos of autonomic dysreflexia
-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)
GBS patho
symptoms
trx
- demyelination of PNS mediated by T and B cells
- ascending weakness or paralysis (can affect resp)
- support, plasmapheresis, Ig
arterial thrombus characteristics:
- begin at site of injury/turbulence
- grow retrograde
- MI - wall (mural) clot
- r/t ATH
characteristics of venous thrombus
- r/t stasis
- prone to embolize
- antergrad growth
- large area of attachment/occlusive
systemic thromboembolism
- starts intracardiac (LV wall, dilated LA)
- goes to LE, brain, GI, kidneys, spleen
- r/t ulcerated plaque or AA
characteristics of pulmonary thromboembolism
- originates as DVT to lungs
- usually multiple
- clinically silent
- > 60% pulm circ occluded = death, CV collapse, CP
DIC
- 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
indicates + Dx of mono
> 50% lymphocytes; 10% atypical lymphocytes (activated)
features of mono
- 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
what genetic abnormality is hallmark for leukemias?
translocation of chrom 9 and 22 (philadelphia chrom)
+ Dx of ALL
->30% lymphoBLASTS
feature of AML
-affects myeloid precursors
features of CML
- chrom 22 (philadelphia)
- polycythemia vera is precursor
- affects myeloid stem cells but presents when mature
features of CLL
-B lymphocytes cannot convert into plasma cells (no fxn)
features of NHL
- cloned B, T, NK cells
- involve mutated proto-oncogenes and TSG
- linked to chrom translocations, infections, environment, immunidef, autoimmune
features of Burkitt’s
- 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
features of poly. vera and treatment
- inc in all blood cells (splenomegaly)
- inc sensitivity to GF
- 4 stages; myelofibrosis and acute leukemia
- hypervolemia
- trx: phlebotomy
anemia of chronic dz
- dec erythrocyte life span
- dec BM response to erythropoeisis (chronic weakened immunity)
- altered iron metabolism
features and types of anaplastic anemia
treatment
- 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
How do you Dx hemolytic anemia and where does it occur?
- Dx: lab tests, BM studies, + inc ERY precursors in BM and in circulation
- occur intravascularly and extra (lymphoid tissues)
which anemias have hgb synthesis problems vs RBC destruction?
hgb synthesis: all anemias except…
destruction: hemolytic, thalassemia, anemias of chronic dz
translocation
crossing over of NON-homologous chroms
nondisjunction
- chromatids fail to separate properly
- occurs in meiosis I or II
- contributes to aneuploidy (trisomy/monosomy gene d/o)
crossingover
- rearrangment of homologous chroms
- occurs in prophas I (before nondisjunction can occur)
