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just a bit more Flashcards

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1
Q

which muscle fibers are oxidative (aerobic) and which are glycolytic (anaerobic)

A

oxidative/aerobic = type I (marathon)

glycolytic/anaerboric= type IIa (sprint)

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2
Q

if a epithelium is to protect against friction what type is it?

A

stratified squamous

–> non keratizinized: moist (esophagus, vagina)

–> keratinized: dry (skin)

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3
Q

if epithelium is for absorption or secretion what type is it

A

simple columnar or simple cuboidal

simple columnar: GI tract (stomach to rectum), uterus

simple cuboidal: small ducts, glands, kidney tubules

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4
Q

if the epithelium is in the lungs or vessels for rapid exchange what type is it

A

simple squamous

-thin for gas and nutrient exhange

in alveoli, capillaries, endothelium

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5
Q

Where is the epithelium stretchy?

A

transitional epithelium
–> only in urinary bladder (bladder and ureters)

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6
Q

what type of epithelium in the respiratory tract

A

pseudostratitifed columnar with cilia

found in nasal cavity –> bronchi

often ciliated and mucus secreting

*once get to alveoli for gas exhange is simple squamous instead

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7
Q

transitional epithelium is only found where in the body

A

exclusively in the urinary tract. It lines the renal pelvis, ureters, urinary bladder, and the proximal portion of the urethra

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8
Q

give the epithelium type of the following

-alveoli, capillaries
-kidney tubules
-GI tract (stomach –> rectum)
-respiratory tract
-skin
-esophagus, vagina
-bladder, ureters

A

alveoli, capillaries = simple squamous

kidney tubules= simple cuboidal

GI tract= simple columnar

respiratory tract= psuedostratifed columnar (ciliated)

skin= stratified squamous (keratinized)

esopaghus, vagina= stratified squamous (non-keratinized)

bladder, ureters= transitional

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9
Q

2 enzymes used in glutathione redox cycle

A
  1. glutathione peroxidase: detoxifies peroxides, removes ROS
  2. glutathione reductase: regenerates reduced GSH using NADPH (from HMP shunt)
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10
Q

enzyme used in glutathione conjugation in phase II detox in the liver

A

glutathione S-transferase (GST)

GSH conjugates with toxins to make the water soluble and to excrete

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11
Q

make glutathione from

A

glycine, glutamate and cysteine

via y-glutamylcysteine synthase and glutathione synthase

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12
Q

p53

A

a tumor suppressor gene

p53–> p21 –> inhibits CDKs if DNA is damaged

found at the G1 –> S checkpoint
(along with Rb)

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13
Q

Rb phosphorylation in G1 phased of cell cycle causes

A

E2F release

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14
Q

cyclins and CDKs in order of cell cycle

G1
G1–>S
S
G2
M

A

G1 phase progression: cyclin D + CDK4/6

G1/S transition: cyclin E + CDK2

DNA replication and G2 prep: cyclin A + CDK2 (S), CDK1 (G2)

M phase entry: cyclin B + CDK1

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15
Q

beta oxidation is just repeated rounds of

A

removing 2 carbon units from fatty acyl CoA

turn the fatty acid into acetyl coA

get NADH and FADH2 to then make ATP

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16
Q

where does fatty acid synthesis vs beta oxidation occur

A

FA synthesis: cytoplasm of liver, adipose, lactating mammary glands

to make acetyl coa–> palmitate (16C)

keep adding 2 carbon units from malonyl coA to elongate via fatty acid synthase

**acetyl CoA is in the mitochondria so need citrate shuttle to get it out

beta ox: mitochondria of liver and muscle

fatty acid –> acetyl CoA + NADH + FADH2

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17
Q

acetyl coa –> malonyl coa for fatty acid synthesis is the rate limiting step

which enzyme and cofactor

A

acetyl coa carboxylase; biotin (B7)

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18
Q

ALT and AST rxns

A

ALT (Alanine Aminotransferase):
Catalyzes the transfer of an amino group from alanine to α-ketoglutarate, forming pyruvate and glutamate.

ALT: ALANINE –> PYRUVATE

AST (Aspartate Aminotransferase):
Catalyzes the transfer of an amino group from aspartate to α-ketoglutarate, forming oxaloacetate and glutamate.

AST: ASPARTATE –> OXALOCETATE

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19
Q

AST and ALT

also know that this is transamination so there will be glutamate and alpha-ketoglutarate too

A

AST: ASPARTATE –> OXALOCETATE

ALT: ALANINE –> PYRUVATE

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20
Q

what cofactor is needed in glycogenolysis for glycogen –> glucose-1-phosphate via the enzyme glycogen phosphorylase (RATE LIMITING)

** G1P will eventually become G6P

A

vitmain B6 (pyridoxal phosphate)

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21
Q

enzymes for glycolgenolyssi final steps

glucose 1 phospahte –> glucose 6 phospahte

glucose 6 phospahte –> glucose

A

G1P –> G6P via phosphoglucomutase

G6P –> G via glucose-6- phosphatase

this allow glucose export to the blood (from liver and skeletal muscle)

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22
Q

fed state (high insulin, low glucagon)

fasting state (low insulin, high glucagon)

what pathways are active

A

fed:
glycolysis (glucose –> energy)
glycogenesis (glucose –> glycogen)
lipogenesis (glucose –> FA –> TAGs)

fasting:
glycogenolysis (glycogen –> glucose)
gluconeogenesis (non carb –> glucose)

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23
Q

where the 3 aortic segments supply

A

ascending aorta: heart via coronary artery

aortic arch: head, neck, upper limbs (via brachiocephalic trunk, left common carotid and left subclavian)

descending aorta: thoracic and abdominal organs, lower limbs

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24
Q

cardiac depolarization

A

Na+ for fast depolarization; in contractile cells (atria, ventricles, purkinje fibers)
-causes phase 0 of AP

Ca2+ for slow depolarization; in pacemaker cells (SA and AV nodes)
-phase 0 in nodal tissue

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25
depolarization in heart
SA node (pacemaker) depolarizes spontaneously due to funny current (If): slow Na+ influx --> threshold --> Ca2+ influx --> AP heart depolarization is triggered by Na+ influx in contractile cells and Ca2+ influx in pacemaker cells, leading to electrical activation and muscle contraction
26
normal ECG findings give all waves and segments
P wave= atrial depolarization PR interval= atrial depolarization + AV nodal delay QRS complex= ventricular depolarization ST semgent= time between ventricular depolarization and repolarization T wave= ventricular repolarization QT interval= ventricular depolarization --> repolarization
27
hypocalcemia vs hypercalcemia impact on heart
hypo= prolonged QT interval hyper= short QT internval QT interval is ventricular depolarization --> repolarization
28
atrial fibrillation on ECG
irregular irregular rhythm with no P wave P wave is atrial depolarization
29
complete mole genetics
all paternal 46XX or 46XY --> empty egg and sperm while a partial mole is 69XXX or 69XXY (maternal and paternal) --> normal egg + 2 sperm
30
hCG in molar pregnancy
high
31
key toxins in streptococcus vs staphylococcus
strep: -streptococcal pyrogenic exotoxins (causes scarlet fever) -streptolysin O and S (beta hemolysis) -hyaluronidase -DNase staph: -Toxic shock syndrome toxin 1 (TSST-1) -exfoliative toxin (causes scalded skin syndrome) -enterotoxins (causes food poisoning) -alpha toxin
32
key of bacteria classification gram-positive cocci gram-negative cocci gram-positive bacilli gram-negative bacilli sphirochetes
gram-positive cocci: staph, strep gram-negative cocci: neisseria gram-positive bacilli: bacillus (aerobic), clostridium (anaerobic), listeria gram-negative bacilli: enterbacteriaceae (e coli, salmonella, shigella), pseudomonas sphirochetes: not visible on gram stain; needs dark field microscopy --> treponema, borrelai, leptospira
33
gram-positive bacilli gram-negative bacilli
gram-positive bacilli: bacillus (aerobic), clostridium (anaerobic), listeria gram-negative bacilli: enterbacteriaceae (e coli, salmonella, shigella), pseudomonas
34
gram-positive cocci gram-negative cocci
gram-positive cocci: staph, strep gram-negative cocci: neisseria
35
purine salvage pathway purpose and enzymes
save energy and reduced uric acid production; recycle free purine bases (adenine, guanine and hypoxanthine) into nucleotides hypoxanthine --> IMP via HGPRT guanine --> GMP via HGPRT adenine --> AMP via APRT
36
HGPRT deficiency is what syndrome
Lesch Nyhan syndrome This deficiency leads to a buildup of uric acid and neurological and behavioral problems. The most characteristic symptom is self-injurious behavior, such as lip and finger biting, and head bangin ------------ Overproduction of Uric Acid: Excess uric acid can lead to gouty arthritis, kidney stones, and other complications. Neurological Abnormalities: Affected individuals experience motor problems, including dystonia (involuntary muscle spasms) and choreoathetosis (involuntary jerky movements). Behavioral Problems: Self-injurious behavior, such as biting and head-banging, is a hallmark of LNS. Cognitive Impairment: While cognitive impairment is present, it can be difficult to assess due to motor disabilities.
37
starting material for pyrimidine synthesis
the first step, catalyzed by the enzyme carbamoyl phosphate synthetase II (CPS II). glutamine, + CO2, + ATP --> carbamoyl phosphate
38
first product of pyrimidine synthesis
UMP (vs purine synthesis is IMP) UMP --> UDP --> UTP UTP --> CTP UMP --> dUMP --> dTMP
39
what factors are defective with vitamin K deficiiency
factor 2, 7, 9, 10 and factor C and S
40
hemophilia A, B and C and what is deficient
A= 8 B= 9 C= 11
41
in von willebrands disease there is a decrease in wWF which leads to a decrease in what other factor
factor VIII (8)
42
thrombotic thrombocytopenia purpura
decrease ADAMTS13 --> increase vWF multimers
43
DIC disseminated intravascular coagulation
widespread clotting --> factor consumption --> increase PT and PTT --> decreased platelets and fibrinogen
44
serotonin synthesis
tryptophan --> 5-HTP --> 5-HT (serotonin) rate limiting is first step via tryptophan hydroxylase
45
glutamate --> alpha ketoglutarate + NH3 kind of transamination rxn; moreso deamination
free ammonia for urea cycle via glutamate dehydrogenase
46
amino acid get broken down into
nitrogen group --> for urea cycle carbon skeleton --> for energy, gluconeogenesiss, ketogenesis glucogenic AAs --> pyruvate or TCA cycle --> glucose ketogenic AAs --> acetyl coA or acetoacetate --> ketones
47
glucogenic vs ketogenic vs both amino acids ***FIND MNENMONIC***
ketogenic: leucine and lysine glucogenic: Ala, Asp, Glu, Ser, Val Both: isoleucine, phenylalanine, tyrosine, tryptophan, threonine
48
what the MARMU of brachial plexus innervate
musculocutaneous (C5-C7): anterior arm (biceps and brachialis) axillary (C5-C6): deltoid, teres minor radial (C5-T1): posterior arm/forearm (extensors) median (C5-T1): most anterior forearm, thenar muscles ulnar (C8-T1): intrinsic hand muscles, some forearm
49
which nerve(s) from brachial plexus has roots from all of C5-T1
radial and median
50
what nerve innervates biceps and brachialis and which for triceps
musculocutenaous triceps= radial
51
what does axillary nerve innervate
deltoid and teres minor
52
types of collagen
type I= bone, skin, tendon, cornea type II= cartilage, type III= blood vessels, uterus, reticular fibers type IV= basement membrane, lens, glomeruli type V= placenta, hair, interstitial tissue
53
classic Ehlers Danlos (hyperextensible skin, joint hypermobilitty) effects what collagen type
type V type III in vascular type
54
alport syndrome (nephritis, hearing loss) and good pasture syndrome (autoantibodies against __ in kidney and lungs) affect what type of collagen
type IV (basement membrane, lens, glomeruli)
55
osteogenesis imperfectă decrease what collagen and 2 key findings
type I blue sclera and bone fragility
56
B9 (folate) vs B12 (cobalamin) and impact on homocysteine and methylmalonic acid
B9: increase homocysteine only B12: increase homocysteine and methylmalonic acid
57
on vs off center cells in eyes
on centers are activated (depolarized) when light hits center of receptive field and inhibited when light hits the surround -->less glutamate in light activates them --> mGluR6 pathway off centers are activated when light hits surrounding and inhibited when light hits the center --> more glutamate in dark causes cells to fire --> inotropic AMPA/kainate glutamate receptors
58
photoreceptors (rods and cones) in dark vs light
dark: depolarized--> release glutamate light: hyperpolarized --> less glutamate
59
light vs dark and glutamate
glutamate in the dark inhibits ON bipolar cells but excites OFF bipolar cells light --> decrease glutamate --> ON bipolar cells activate, OFF bipolar cells deactivate
60
mydriasis
pupil dilate to let more light in eye SNS; NE via dilator pupillae muscles
61
mydriasis vs mitosis
mydriasis= pupil dilate SNS mitosis= pupil constrict PNS
62
mitosis
pupil constriction to protect retina from bright light PNS and Ach sphincter pupillae muscle
63
muscle for mydriasis (pupil dilate) vs mitosis (pupil constrict)
mydriasis= SNS; NE via dilator pupillae muscles mitosis= PNS; Ach via sphincter pupillae muscle
64
weber and rinne for sensorineural and conductive hearing loss
weber to the worse (conductive): weber lateralizes to affected ear in conductive hearing loss weber to the better (sensorineural): weber lateralized to unaffected ear in sensorineural loss rinne= AC>BC is right (normal or sensorineural) rinne= BC>AC is wrong (conductive)
65
substantia nigra
in midbrain and part of basal ganglia system movement control an dopamine production pars compacta: voluntary movement; dopamine pars reticulata: motor output inhibition; GABA
66
2 divisions of the substantia nigra to modulate movement
pars compacta: voluntary movement; dopamine pars reticulata: motor output inhibition; GABA
67
pars reticulata în basal ganglia of substantia nigra
for motor output inhibition via GABA helps to regulate eye movement too
68
direct vs indirect pathway of the basal ganglia to regulate movement initiation and inhibition
direct pathway: for movement; D1 dopamine receptor indirect pathway: inhibit movement via D2 dopamine receptor ; double negative
69
GPe and GPi (globus pallidus externa and interna) in the direct vs indirect pathway of basal ganglia for movement regualtion
GPe is only in indirect pathway and it inhibits the Stn --> promotes movement when active Gpi is in direct and indirect pathway --> inhibits thalamus and inhibits movement when active
70
direct pathway vs indirect pathway of basal ganglia for movement regulation
* Direct Pathway ("'Go") * Facilitates movement * Dopamine stimulates D1 receptors in the striatum * Striatum inhibits GPi/SNr * GPi/SNr inhibits thalamus less → thalamus activates cortex * Promotes movement * Indirect Pathway ("No-Go") * Inhibits movement * Striatum inhibits GPe * GPe normally inhibits STN → so now STN is disinhibited * STN stimulates GPi/SNr * GPi/SNr inhibits thalamus more → cortex activation reduced * X Suppresses movement Dopamine (via D2 receptors) inhibits the striatum - this reduces the indirect pathway → less inhibition of movement → promotes movement
71
which 2 conditions have cherry spot of macula and both in ashkenazi jewish a lot and which also has hepatosplenomegaly
tay sacs= cherry spot Neumann pick= hepatosplenomegaly plus cherry spot
72
tay sachs vs Niemann pick disease
tay sachs - HexA deficient -cherry spot on mutual -neurodegeneration -onion skin appearance -ashkenazi jewish neimann pick -sphingomyelinase deficient --cherry spot on mutual -neurodegeneration -foamy macrophages -hepatosplenomeglay -ashkenazi jewish
73
eicosanoids are made from
arachidonic acid eicosanoids= prostaglandins, thromboxane, leukotirenes, lipoxins
74
phospholipase A2
release arachidonic acid from membrane phospholipids
75
low dose vs high dose dexamethasone test for cushing disease
low dose -normal= cortisol suppressed -cushing= cortisol not suppressed high dose - pituitary problem (cushing)= cortisol suppressed -ectopic ACTH or adrenal tumor= cortisol not suppressed dexamethasone:: to suppress the release of ACTH (adrenocorticotropic hormone) from the pituitary gland.

NPLEX (44 decks)

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