NBME Flashcards
(144 cards)
1
Q
What is apoptosis characterized by
A
cell shrinkage, nuclear shrinkage, (pyknosis) and basophilia, and membrane blebbing, nuclear fragmentation (karyorrhexis) and formation of apoptotic bodies which are then phagocytosed
2
Q
pyknosis
A
nuclear shrinkage
3
Q
karyorrhexis
A
nuclear fragmentation
4
Q
basophilia
A
a dye (basic or positive) that stains DNA/RNA in the nucleus, RNA in ribosomes, which are acidic and negatively charged
5
Q
what is the intrinsic pathway?
A
involved in tissue remodeling in embryogenesis
occurs when a growth factor is withdrawn from a proliferating cell population,
occurs after exposure to injurious stimuli radiation, toxins hypoxia
changes in proportions of anti and pro apoptotic factors lead to increased mitochondria permeability and cytochrome C release
6
Q
extrinsic pathway
A
FAS ligand binding to FAS
immune cell 9perforin and granzyme B
7
Q
necrosis
A
enzymatic degradation and protein denaturation resulting from irreversible injury
intracellular components extravasate
inflammatory process
8
Q
coagulative necrosis characteristics
A
eosinophilia, loss of cytoplasmic and nuclear detail, blurring of cytoplasmic membranes, cell otherwise intact preservation of tissue architecture
9
Q
reversible with O2
A
decreased ATP synthesis
cellular swelling ( no ATP —> impaired Na+/K+ pump)
nuclear chromatin clumping
decreased glycogen
fatty change
ribosomal detachment (decrease protein synthesis)
10
Q
irreversible cell injury
A
nuclear pyknosis, karolysis, karyorrhexis, Ca2+ influx, –> Capsase activation
Plasma membrane damage
lysosomal rupture
mitochondrial permeabillity
11
Q
red infarcts
A
red infarcts occur in tissues with collateral circulation,
liver lungs, intestine
12
Q
pale infarcts
A
sold tissues with single blood supply
heart kidney and spleen,
13
Q
Clinical presentation of hypovolemic and cardiogenic shock
A
low output failure
increase TPR
low cardiac output
cold clammy patient, vasoconstriction
14
Q
Clinical presentation of septic shock
A
high-output failure
decreased TPR
dilated arterioles, high venous return,
hot patient (vasodilation)
15
Q
atrophy
A
decrease hormones (uterus/vagina) decrease innervation (motor neuron damage) decrease blood flow decrease nutrients increase pressure (nephrolithiasis) occlusion of secretory ducts
16
Q
Clinical Presentation of Inflammation
A
redness, dolor, calor, tumor, loss of function
17
Q
vascular component of inflammation
A
increase vascular permeability, vasodilation, endothelial injury
18
Q
cellular components of inflammation,
A
neutrophils extravasate and participate in inflammation, phagocytosis, degranulation and inflammatory mediator release
19
Q
acute inflammation
A
rapid onset
lasts minutes to days
20
Q
key players in acute inflammation
A
neutrophils
21
Q
chronic inflammation
A
lymphocytes and macrophages
characterized by persistent destruction and repair
blood vesel proliferation and fbirosis
22
Q
granuloma
A
nodular connections of epithiliods and giant cells, outcomes include scarring and amyloidosis,
23
Q
outcomes of acute inflammation
A
complete resolution abscess, or progression to chronic inflammation
24
Q
causes of acute inflammation
A
infection
necrosis
physical injury
25
causes of chronic inflammation
autoimmune disease
chronic irritation
viral infecton
26
systemic inflammation of acute inflammation
chills,
fever,
myalgias
27
From blood to sites of tissue injury, neutrophils via 4 steps
rolling,
adhering,
diapedsis,
migration
28
which protein allows neutrophils to roll?
selectins
29
which protein allows neutrophils to adhere
integrins
30
what do leukocytes use to travel through interstitium
chemotatic signals`
31
free radicals damage ]
membrane lipid peroxidation,
protein damage
and DNA breakage
32
where do free radicals come from?
```
gamma rays and x rays,
metabolism of drugs
redox reactions
NO
transition metals,
leukocyte oxidative burst
```
33
Elimination of free radicals
```
catalase
superoxide dismutase,
glutathione peroxidase
spontaneous decay
antioxidants
```
34
retinopathy of prematurity
abnormal blood vessels grow in the retina, retinal detachment -->causing blindness
35
bronchopulmonary dysplasia
in premature infants, chronic lung disease caused by mechanical ventilation and oxygen supply.
36
wound healing
| three stages
inflammatory
proliferative
remodeling
37
inflammatory key mediators
platelets, neutrophils, and macrophages
38
proliferative key mediators
fibroblasts, myofibroblasts, endothelial cells, keratinocytes, and macrophages.
39
remodeling key players
fibroblasts
40
what occurs during inflammation
increased vascular permeability, clot formation, neutrophil migration, macrophage clean up debris 2 days later
41
what occurs during proliferation
deposition of granulation tissue and collagen, angiongenesis, epithelial cell proliferation, dossolution of clot and wound contraction mediated by myofibroblasts.
42
what occurs during remodeling
type III collagen replaced by type I collagen
| increase tensile strength of tissue
43
transudate
hypocellular
protein poor
specific gravity < 1.012
44
exudate
cellular
protein rich
specific gravity >1.020
45
cause of exudate
lymphatic obstruction
| inflammation
46
causes of transudate
increased hydrostatic pressure
decreased oncotic pressure
Na+ retention
47
caseating granuloma
| Dx
TB
48
noncaseating granuloma
```
Tb
sarcodoisis
other infections
foreign material
fungal infections
```
49
Increase erythrocyte sedimentation rate
| is an indicator of?
```
infections,
inflammation
cancer
pregnancy
SLE
```
50
decrease erythrocyte sedimentation rate
sickle cell
polycythemia
CHF
51
Symptoms of iron poisoning
acute, gastric bleeding
| chronic metabolic acidosis, scarring leading to GI obstruction
52
metaplasia often the result
secondary to irritation and/or environmental exposure
53
dysplasia
abnormal growth with loss of cellular orientation, shape, and size in comparison to normal tissue, maturation; commonly preneoplastic.
54
which plasia's are reversible
hyperplasia,
metaplasia,
dysplasia
55
anaplasia
abnormal cells lacking differentiation, resemble primitive cells of same tissue, often equated with undifferentiated malignant neoplasms, little or no resemblance to tissue of origin.
56
neoplasia
a clonal proliferation of cells that is uncontrolled and excessive.
may be benign or malignant
57
Barret's esophagus,
change from squamous cell adenocarcinoma to esophageal adenocarcinoma.
58
BCL2
follicular lymphoma and undifferentiated lymphoma,
anti apoptotic molecule,
BCL2 sensors,
BCL2 inhibit the sensors, which prevents mitochondria from releasing cytochrome C and activates capsases.
59
aflatoxins are associated
| with what cancer
hepatocellular carcinoma
60
Asbestos
mesothelioma
61
how is volume of distribution impacted with kidney or renal disease
Vd is increased
62
describe the characteristics of a drug with high Vd
lipid soluble, low protein binding, low rates of ionization
63
equation for half life
.7x Vd/Cl
64
Bioavailability
fraction of drug that reaches systemic circulation unchanged
65
Equation for the volume of distribution
total amount of drug/ plasma drug concentration
66
Acetaminophen toxicisity
| classical presentation
hepatoxicisity
67
hepatoxicisty what lab value would indicate liver damage
ALT
68
What is the cause of acetaminophen toxicisity
N-Acetyl Para Benzoquinoneimine
69
acetaminophen overdose situation
more drug is available for CYP metabolism to a toxic metabolite.NAPQI
70
what metabolizes the toxic metabolite of acetaminophen
glutathione,
71
glutathione is a combination of
glutamate, cysteine, and glycine
72
what enzyme catalyze formation of glutathione conjugates?
glutathione S transferase
73
what increases
| the risk of acetaminophen hepatotoxicity?
alcohol inducible CYP2E1 which rapidly forms NAPQI'
malnutrition decreases GSH and UDP glucoronic acid levels
high acute doses, >10grams in adults
74
Stages of Acetaminophen toxicisity
stage 1
stage 1 (0-24 hours)
patients are often asymptomatic,
nonspecific symptoms,
nausea vomiting, lethargy, drowsiness, diaphoresis,
75
Stages of Acetaminophen toxicisity
stage 2
patients are often asymptomatic,
mild increases AST
and some right upper quadrant pain
76
Stages of Acetaminophen toxicisity
stage 3
```
AST, ALT levels > 10,000IU/ml
fulminant hepatic failure
encepholapthy, coma
hemorrhage,
jaundice
liver transplantation may be needed renal changes usually less prominent.
```
77
Stages of Acetaminophen toxicisity
stage 4
liver regernates, near normal laboratory values often observed within a week.
complete recovery may take months
78
what's the treatment of acetaminophen toxicisity
NAC
79
acute management
| of acetaminophen
activated charcoal, if you know its toxic
get blood samples, >4 hours and less than 24 hours after dose,
give it if its above treatment line in the Rumack matthew noomogram
80
Why NAC works
it's a source of systeine to form glutathione
some binds directly to NAPQI
source of sulfate for sulfate conjugation
81
list the following G proteins and what's it linked to
alpha 1---> Gq
alpha 2 ---> Gi and Go
B1 B2 B3, D1---> Gs
82
D1
produce dialtion of renal arteries
83
LOCATION OF B1 RECEPTORS
heart and kidneys
84
B2
heart and produce inhibitory effects of sympathetic stimulation
85
B3
lipolysis
86
competitive antagonists
| on efficcacy grraphs
shifts curve to the right, decrease potency, no change in efficacy
87
noncompetitive antagonist
shifts curve down, decreases efficacy.
| can't be overcome by increasign agonist substrate concentration,
88
what is a great example of noncompetitive antagonists
phenoxybenzamine on alpha receptors
89
partial agonsits,
decreases efficacy
90
therapeutic index
a comaprison of hte amount of therapeutic agent that causes the therapeutic effect to the amount that causes toxicisity
91
analogy to remember the equation for TI
TILE
Therapuetic index= LD50/ ED50
lethal dose/ effective dose
92
therapeutic window
refers to range of doses which optimize between eficacy and toxicisity
93
what does higher TI values?
SAFER DRUGS
94
which receptor causes mydriasis
alpha 1
95
what causes vascular smooth muscle contraction
alpha 1
96
what causes intestinal and bladder sphincter muscle contraction
alpha 1
97
what works in the CNS and decreases sympathetic outflow
alpha 2
98
what causes increase in platelet aggregation
alpha 2
99
what causes bronchodilation
Beta 2
100
what causes vasodilation
beta 2
101
phenelyphrien is use to treat
mydriatic agent and decongest agent
102
albertorl terbutaline metaproterenol, salmeterol
formoterol
act on what receptor and are used for what?
Beta 2,!!!!!!
| bronchodiltion, in asthma and COPD
103
Norepinephrine treats
acute hypotension HYPO
104
adverse side effects of alpha agonists
hypertension and cerebral hemorrhage
105
adverse side effects of beta agonists
tremor and nervousness, tachycardia, and palpitations
106
main use of reserpine
blocks VMAT, ultimately depleting NE from terminals,
| main use is to treat hyperkinetic movement disorders,
107
main use of ephedrine
releases NE and is a direct agonist
| treats hypotension and nasal congestion
108
pseudophedrine
nasal decongestant
109
phenoybenzame
only noncompetitive blocker
110
phentolamine
prototype
111
alpha 1 selective
prazosin, doxazosin, terazosin
112
to manage pheochomocytoma
phenozybenzamin
113
to treat BPH,
urinary obstruction BPH!!!
114
why with alpha antagonists do you get tachycardia
excess norepinephrine release
| but mainly, you lose the control found on alpha 2 receptors which are autoreceptors.
115
what increases outflow of aqueous humor
alpha agonist
116
what decreases secretion of aqueous humor?
beta blockers
117
beta blockers that reduce the production of aqueous humor
timolol betaxolol
118
What's used to reduce the myocardial infarction?
propanolol
metaprolol
timolol.
119
what's used to treat congestive heart failure
metoprolol carvedilol
120
adveser effects of beta blockers
heart failure
arrythmias
don't use with patients iwth asthma
121
ganglionic blockers
blocks nicotinic receptors in ANS ganglia,
| Destroys ANS,
122
choline esters
ACh, methacholine, carbachol, bethanechol
123
characteristics of choline esters
poorly absorbed from GIT and doesn't cross BBB
124
which ones excite nicotinic receptors
ACh, and carbachol
125
which drugs have a longer duration of AChE?
carbachol and bethanechol
126
what are alkaloids?
pilocarpine,
127
alkaloids are better than cholines
because they are well absorbed from GIt, and they do cross BBB
128
Pilocarpine,
selective for muscarinic receptors.
129
two mechanisms of muscarinic agonists
direct stimulation of muscarinic receptor
| stimulation of muscarinic receptors on presynaptic terminal to reduce release of neurotransmitter
130
direct acting cholinometics on the vasculature
dilation via nitric oxide
131
methacholine
diagnosis of asthma
132
pilocarpine
xerostomia and glaucoma
133
Bethanecol
postoperative ileus and urinary retention
134
carbachol
glaucoma
135
contraindications of muscarinic directing acting drugs
asthma or cOPD
obstruction in GIT or urinary system
bradycardia hypotension
hyperthyroidism
136
what's the good thing about edrophonium
lasts only 2-10 minutes
137
what's good about carbamic acid esters?
neostigmine, physostigmine pyridostigmine, block up to 6 hours of ACHE
138
organophosphates?
echothiopate and malathion
139
echthiopate
glaucoma
140
physostigmine
glaucoma, antimucarinic drug intoxication
141
edrophonium
diagnosis of MG , reversal of neuromucular blockade
142
pyrdistigmine and ambenonium
treatment of MG
143
neostigmine
postoperative ileus and urinary retention, MG, reversal of neuromuscular blockade
144
muscarinic adverse effects
```
weakness or paralysis
increased sweating
diarrhea
vomiting
miosis
bronchial constriction?
```
