amboss incorrects Flashcards
1
Q
how to differentiat between toxo retinitis and cmv retinitis
A
cmv=floaters/encephalitis,esophagitis/pneumonitis toxo however-causes eye pain/retrochoritdits, and fluffy lesions
2
Q
noise induced hearing loss
A
destruction of cochelar hair cells
3
Q
otoscleooris
A
chl mostly bilateral 3rd and 4th decade of life
4
Q
acoustic neuroma
A
tinnitus gait instability
5
Q
l4 herniation vs l5 herniation
A
decreased patella l5 decreased achilles
6
Q
where is subependymal giant cell astrocytoma seen
A
TSC
7
Q
oxygen induced retinopathy
A
inhibits vegf formation
8
Q
common casses of meningioma
A
falx cerebri and spehnoid and foramen magnum
9
Q
where does medulloblastma originate form
A
primitive neuroectoderm
10
Q
what do arachnoid cells gve rise to
A
meningiomas
11
Q
what do astroglial cells give rise to
A
astrocytomas
12
Q
lymophocytic infiltrate of endoneurium seen in
A
gullian barre syndrome
13
Q
MS is caused by which cells
A
th1 react to myelin basic protein=focal demyelination
14
Q
what does mononeuritis simplex present as
A
painful sensory/motordefect it occurs in vasulitis
15
Q
inhibition of 5ht /NE reuptake
A
amitryptiline
16
Q
what alters perception of ascending pain impulse what is effect of opiod
A
vasodilation
17
Q
what is there in alway s aneurologic stroke
A
PAINLESS FOCAL NEUROLOGIC DEFICIT
18
Q
what is a complication of axillar node dissection
A
long thoracic nerve injury
19
Q
what happens in excessive alcohol biochemically which enzyme fucked
A
pyruvate dehyrdogenase
20
Q
clinical features of G6pd
A
Clinical findings include yellow-tinted skin, dark urine, and fatigue
21
Q
advese effects of acetolazimide
A
sulfa allergy,hypokalemia and phyperamminome
22
Q
why does acetolazimide cause hyperammoniema
A
cause inorder for ammonia to be excreted with need
23
Q
all diuretics chave one adverse effect
A
hypokalemia
24
Q
neurocyterosis vs toxoplasmosis how to differentiate
A
the latter one needs hiv
25
hyperammoniemia induced encephalopathy
astrocytes detoxify ammonia(glut dehydrogenase) and glutamine synthease water moves into cells=cerebral edema
26
worsening character for trochlear nevr lesion
downward gaze
27
a patient comes with confusion ataxia and mamillary body
wernicke
28
where do you see intraparenchymal cyst
neurocyticrosi
29
brainstem glioma
NF1, seixures cafe au lait
30
CJD classic symtooms
akinetic mutism/neuropsyhcatric symtoms
31
myoclonic jerks part of which isease
merrf mutation in mt k gene opsoclonus myoclus sundrome=myoclong jerks and atasia/ seen in neuroblastma as well
32
adenoma sebaceum seen in
tuberous sclerosis present with ataxia and nystagmus? hamartoma in cerebellum or subependymal astrocytoma causing hydrocephalus
33
beta amylkoid 1 42
alzehimers disease indicator
34
anti gangloside ab
gulian bare
35
what is the most common cause of anti yo antibodies
breast cancer
36
what produces anti nmda and anti hu
ovarian teratoma and small cell lung cancer
37
what causes hyperphosphrylation of tau
glycogen synthae 3
38
which nerve courses along parotid gland
facial nevr, does it innervate/ no
39
whiplash injury
central cord syndrome
40
a pregnant woman has toxoplasmosis infection what would you find on the baby
the baby would have spasticity of the lower leg with hydrocephalus
41
whend o msk nerve injury occurs
due to heavy liftint typically
42
a person has mengitis with gram + bacillis surrounded by rim what is it
listeria
43
what drugs cause glaucoma
atropine
44
how to dy/dx polymyositis with myasthenia gravis
polymyositis ocular muscles never affected
45
what causes spontaneus ruptures in the brian
amyloid angiopathy, causes microaneurysms which could rupture and result in stroke
46
what do flurionated anestheritc shave in common
they all increase in cerebral blood flow
47
what is alpha synuclein misfolding
parkinsons
48
typical locations of brain tumors
49
risk factors for ICH of newborn
\<32 weeks
hypoxia
chorioamniotis
Infection of the amniotic fluid, fetal membranes, and placenta that is most commonly due to ascending cervicovaginal bacteria (e.g., Ureaplasma urealyticum or Mycoplasma hominis)
50
why do we have high arched palate in mytonic dystrophy
reducesd temporalis and ptyergoid muscle growth
51
how can subfalcine herniation cause hydrocephalus
it compresss foramen monro
52
brown sequard lesion
53
what is chromatolysis
A reaction of a neuronal cell body in response to an axonal injury; it is characterized by swelling of the neuronal body, dispersion of the Nissl bodies, and displacement of the nucleus to the periphery.
54
55
how does fish bone in pyiriform fossa fuck up laryngeal nerve
The superior laryngeal nerve divides into an internal and external branch beneath the internal carotid artery. The internal laryngeal nerve runs directly beneath the mucosa of the piriform recess, along with the recurrent laryngeal nerve, and is distributed to the mucous membrane of the larynx. The internal laryngeal nerve can be injured during surgery (e.g., thyroidectomy) or damaged by food items (e.g., a fishbone) being trapped in the piriform fossa. Damage to this nerve classically manifests with an impaired cough reflex, which increases the risk for recurrent aspiration pneumonia.
56
how does thambutol act
The mechanism of action of ethambutol is the inhibition of arabinosyltransferase, which subsequently inhibits the synthesis of arabinogalactan, an important mycobacterial cell wall polysaccharide
57
mercury posioning how he looks
buccal inflamation, blue white discolouration/ployneuropathy
58
diagnosis of narcolepsy which wave
periodic sharp waves seen in
old ppl
delirum
rapid onset of beta waves
cjd
delta waves decreased in old people
diffuse slow waves=delirum
59
can pregnant woman develop wernicke encephalopathy
yes metabolic demand of thiamine/ increaed hypermesis gravidarum
60
what are radial glial cells
A collection of nonspecific, reactive changes (e.g., proliferation, hypertrophy) to glial cells in response to CNS damage
line the ventricles
what is glial scleoriss
61
a pupillary dilator agonist increases nor e release what is it
ACH from preggl neuron, causes contractin of pylorus
62
inflammation of chorid plexus
Inflammation of the choroid plexus (choroid plexitis), which is most commonly caused by CNS infection (e.g., tuberculosis, cryptococcosis) can result in increased CSF production and thereby cause lateral ventricle enlargement, as seen here on the T2 weighted MRI. However, this patient does not have any clinical features of CNS infection (e.g., fever, headache, meningism) and there is no enlargement of the choroid plexus in the lateral ventricles on imaging to suggest choroid plexitis.
63
non communicationg hydrocephalus causes
Obstruction of the foramen of Monro, which is typically caused by a tumor (e.g., colloid cyst), would result in unilateral (asymmetrical) lateral ventricle enlargement, unlike this patient who has symmetrical enlargement of both the lateral ventricles on the T2 weighted MRI.
64
what is high pitched pericardial knock
early pericardial lesion which is high pitched occurs early diastole
65
temporal arteritis to development of thoracic aneurysm
lets say 10 years
66
why hand clenching increases vsd murmur
increased afterload therefore increase L-R shunt which causes systolic sound (holosystolic)
67
why ASD has systolic ejection murmur
why ASD has soft midiastolic murmur
Relative pulmonary stenosis due to an increase in stroke volume
Soft mid-diastolic murmur over the lower left sternal border
68
what is differential cyanosis / reverse dy/dx cyanosis
The reversal of the shunt results in a mixture of deoxygenated and oxygenated blood reaching the lower extremities.
reverse is the opposute
69
a continuous murumur that become loud on the second heart sound is
PDA
70
what is brugada syndrome
present as syncope with tacchyarthmia
incolmplete RBBB, and elevation in v123
71
a person is alcoholic takes diuretics and has diarrhea he develops torsades des pointes why?
hypomagensemia
which diruetics
loop
72
where is the aortic isthmus what are the symotoms
is located just distal to the origin of the left subclavian artery and is tethered by the ligamentum arteriosum
(hematoma seen on the chest typically hand sized)
however if injury to IVC it can result in (retropertioneal bleed)
73
if you have injury to aortic isthmus if coronary artery injured how would it manifest as
increased st segment
74
how can presence of vasopsatic angina be confirmed
coronary angiography with ACh released
75
HCMo is highly variable why?
in restrictive cardiomyoapthy MOA of death
remember one thing aortic stenosis never results in sudden cardiac death why
some patients develop symmetric however other patients are asyymetric
not sudden
because it manifes as SAD
76
what other disease can cause lebiman sack endocarditis
are libeman sack endocarditis dangerous
a person has fever and new murmur what it ocould eb
advanced cancer /rheumatoid arthiritis
it is dangerous since it can be dislodged and embolizied
infective endocarditis
77
what is exactly coarctation of aorta medial and intimal hypertrophy causes narrowin preductal and postfuctal types of cyanosis and when does rib notching occur
what are the symotoms of coarctation of aorta
rib notching doesnt occur before 5 years
dyx cyanosis can occur delayed towards the leg, if subclavian artery involved will lead to high right arm pa anddifferential cyanosis of the the right arm
LVhypertrophy and symptoms dont produce in utero because of Patent ductus arteriosus
78
where and why do you hear murmur of coarctation of aorta
Systolic ejection murmur over left posterior hemithorax
becausestenosis of aorta there
continous murmur b/w scapular space due to collateral flow
79
what are the consequeunces of brachial hypertension
headache eppxistasix and tinnitus
80
what happens if in coartcation PDA suddenly closes
it can cause hypotension and shock
81
wjhy we have pericarditis after neutrophilic inflammation
e.g., TNF-α, IL-2, IL-6) from neutrophils causes exudation of fibrin and leukocytes into the pericardial space, resulting in fibrinous pericarditis.
82
EARLY MI
late mi
release of cytokines from cells, early recruitment of neutophils can lead to motlling
hypercontraction of myofibrils
and after 12 24 hours dark mottling
if contraction band it is repurfusion injury
83
what is the MOA of prostacyclin analogs
ncreased activation of protein kinase A is the mechanism of action of prostacyclin analogs, a class of drugs used to treat pulmonary hypertension. Prostacyclin analogs bind to prostacyclin receptors and activate G protein, which in turn stimulates adenylyl cyclase, resulting in increased intracellular cAMP. Intracellular cAMP activates protein kinase A, which causes vasodilation by inhibiting myosin light chain kinase, the structure responsible for smooth muscle contraction. Ho
84
why we dont have JVD on normal inspiration
During inspiration, there is increased systemic venous return and increased volume in the right heart, which is compensated for by expansion into the pericardial space
85
which conditions leads to high A wave
when is v wave seen
A prominent a wave may be seen in patients with right ventricular hypertrophy or pulmonic stenosis
seen in tricuspid regurgitation and right heart failure. This patient's v wave should not be significantly changed.
86
what is holiday heart syndrome
particular, acute alcohol consumption often triggers paroxysmal A-fib (also known as “holiday heart syndrome”), which subsides within 7 days without intervention
presens with syncope and dizziness
87
why do you have JVP in constirctive vs tamponade u dont
noncompliant ventricle doesn expand
tamponade-imapired rv filling due to cardiac compression
when does jvp occur only in poulsus paradoxus
88
Pulmonary artery hptn
pcwp lfh
\>25
\>18
89
What does RHF lead to in kidney
what is coronary sinus dilation
Right heart failure is a condition that can cause systemic hypoperfusion. For this reason dilatation (not constriction) of the renal afferent arteriole would rather be expected in this patient.
Reduced right-sided cardiac output leads to venous congestion in the vessels that drain into the right heart, including the coronary sinus, which can become dilated as a result
90
how do nitrates work
when are they contraindicated
Nitrates work by forming free radical nitric oxide,
rhf, HCOM
91
side effects of exitimidbe
hepatotoxicity
92
Developed countries
radiastion therapy dangerous
93
mutation in fibrillin
predispose to mucoid extracellular matrix accumulation, medial fibrosis, and loss of smooth muscle cell nucle
94
Pressure gradient location in aortic stenosis vs HCOM
HCOM is below aortic valve wheras aortic stenosis across aortic valce
95
is thrombosis of bowel common or emboli
if emboli where does it occur
emboli mor comomon,sma/ima
96
IN ami how are the coronary arteries
how nitroglucerin improves venticular compliance
they are in acute state of dilation due to impaired o2 delivery Nitroglycerin actually improves ventricular compliance by reduction of myocardial preload and its effects.
97
what features confirm diagnosis of TOF
Echocardiography showing a pulmonary artery arising from the left ventricle and aorta arising from the right ventricle confirms the diagnosis of transposition of the great arteries,
98
why high cardiac output causes volume overload
However, despite increased cardiac output, low systemic vascular resistance results in arterial underfilling, decreased renal perfusion, and retention of salt and water, which leads to volume overload and heart failure.
99
when is d dimer test used in DVT
to rule out DVT in low pretet probability
100
stasis dermatitis
n inflammatory skin condition characterized by a scaly, pruritic rash on the lower extremities. Most commonly occurs as a consequence of chronic venous insufficiency and edema.
101
cholestrol embolization syndrome
This patient presents with the classic symptoms of blue toe syndrome, livedo reticularis, and acute kidney failure. Eosinophilia and eosinophiluria in the setting of cholesterol embolism are very suggestive findings.
102
action of fibrates
Fibrates are associated with an increased risk of cholesterol gallstones because they inhibit the cytochrome p450 enzyme cholesterol 7-α hydroxylase (↑ cholesterol and ↓ bile acid concentration in bile
103
why do we have tet spells
which CHD cause pulmonary congestion
due to contractions of infinduibular septum, how to manage it beta blockers, volume expansion and iv morphinet
runcus arteriosus, total anomalous pulmonary venous return)
104
TAPVR
how could it cause pulmonary edema
All four pulmonary veins drain into the systemic venous circulationminsted of there could be a right to atrial shunt
obstruction of pulmonary vein =pulmonary congetion
Pulmonary venous obstruction: obstruction of pulmonary venous return → ↑ pulmonary venous pressure → ↑ pulmonary edema → ↑ PVR → RVH, ventricular dilation, and heart failure
105
perioral parethesia is side effect of antiarrythmic drug
and sedation
Perioral paresthesia is a side effect of lidocaine, a class IB antiarrhythmic agent used to treat ventricular tachycardia.
Sedation is a known side effect of beta blockers (e.g., metoprolol, labetalol) and class IB antiarrhythmics (e.g., lidocaine, mexiletine). These agents are lipophilic and can penetrate the blood-brain barrier, resulting in CNS side effe
106
Great saphenous vein coryse
The great saphenous vein (GSV) originates at the base of the hallux, continues proximally by passing anterior to the medial malleolus and then courses along the posterior aspect of the medial femoral condyle before running deep into the thigh to join the femoral vein.
107
inhaled NO
nhaled nitric oxide (NO) is the mainstay treatment for PPHN because of its ability to potently vasodilate the pulmonary vasculature (reducing V/Q mismatch) without decreasing systemic vascular resistance.
108
PDA=
pvr in relationt o hypovolemic shock
a continuous machinery murmur best heard in the left infraclavicular area.
include an increased respiratory rate (as a compensatory response to lactic acidosis) and increased alveolar-capillary permeability.
109
The antitoxin can only neutralize unbound toxin and should therefore be administered early in the course of the dise
110
whats the difference in lovation b/w mVP and mitral regurgtation
one radiates to acxilla, the other is associates to 5th intercostal space
111
how do statins cause myalgia MOA
Statins can decrease the synthesis of coenzyme Q10 and impair energy production within muscle, which can result in myalgia, muscle weakness, and increased serum creatine kinase (CK)
112
causes of increased tags
serum triglyceride concentrations include beta blockers, glucocorticoids, cyclosporine, and some HIV antiretroviral drugs.
113
what will hemopericardium due to MI cause
Px of free wall rupture
PX of interventricualr septum
Ventricular wall rupture can occur within 2 weeks of myocardial infarction and typically results in hemopericardium and cardiac tamponade, which can manifest with profound right heart failure, shock, and often death.
so its symptoms are of obstructive shock
new-onset chest pain and cardiogenic shock due to cardiac tamponade.
signs of RHF
114
explain pathophys cardiorenal syndrome
Systolic dysfunction → reduced cardiac output → renal hypoperfusion → prerenal kidney failure
Diastolic dysfunction → systemic venous congestion → renal venous congestion → decreased transglomerular pressure gradient → ↓ GFR → worsening kidney function
RAAS activation → salt and fluid retention → hypertension → hypertensive nephropathy
115
where would thrombus of abdominal aneurysm normally occur
Occlusion at the opening of the IMA by a thrombus within an aortic aneurysm (suggested by the filling defect) would cause acute mesenteric ischemia and, potentially, necrosis of the bowel segments supplied by this artery
116
how does ACE inhibitor cause reoaxtaion moa
Angiotensin-converting enzyme (ACE) inactivates bradykinin, an inflammatory mediator that increases intracellular calcium in endothelial cells. Intracellular calcium stimulates nitric oxide synthase to convert arginine to nitric oxide, which mediates the relaxation of vascular smooth muscle cells to cause vasodilation.
117
why isnt heparin used for long term treatment
it is only adminstred subcutaneously requires monitoring
118
timiolol is passively absorbed into the eyse
119
why thiazides good for salt secretion
causes hyponatremia due to decresed salt but increased water absorption however loop diuretics destroy the gradient so technically hypernatremia
120
thyroid artery
what lies posterior to esophagus
which CCB blocker cause Peripheral edema, which causes gingival hyperplasia
sup-eca
inf-thyrocervical trunk
include the thoracic duct and azygos vein.
PE=amlodipine
GH-non dihydropyridine
121
Granulomatous nodules on mitral valve is
Formation of giant cells in the tunica media is characteristic of giant cell arteritis (GCA) and Takayasu arteritis, both of which are large vessel vasculitides and can result in an AAA. H
Granulomatous nodules on the mitral valve are associated with rheumatic heart disease (RHD
122
what causes intrapulmonary shunting
\where it occurs
Some common conditions that can cause intrapulmonary shunt include pulmonary AVM, hepatopulmonary syndrome, severe cases of pulmonary edema, and lobar atelectasis.
perfusion no ventalation
123
what causes arthesosclerotic plaque to rupture
marfan syndrome how does it look on ct/arthropathy
increase metalloproteinase
which causes thrombus to form over
with Marfan syndrome have hypermobile joints, which predisposes them to chronic arthralgia as a result of recurrent sprains, bursitis, and/or early-onset osteoarthritis. Cystic medial degeneration,
124
prolonged qt interval
Prolongation of the QTc interval is a possible ECG change seen on cardiac stress testing in patients taking class IA and class III antiarrhythmic drugs, which block potassium channels, resulting in a prolonged repolarization phase of the cardiac action potential. Flecainide has minimal effects on the ventricular repolarization but can result in shortening (rather than prolongation) of the QTc interval on stress testing.
125
what heart sound would be expected in aortic stenosis
Moreover, in aortic stenosis, a paradoxical split of S2 would be expected on cardiac auscultation rather than a wide splitting of S2.
126
why pulmonary edema has bats wing appearence
compare ards with PE
In pulmonary edema, the opacification can often assume a perihilar distribution (a so-called “batwing” or “butterfly-shaped” pattern), which is seen here, because the periphery of the lung has better lymphatic drainage than the central regions
127
pathogensis of thromboarteries
infolatmition of intima, neutrophil migration microabscess formation
interal elastic lamina remains intact
128
limiing factor of coronary blood flow
excercise
129
isruption of an atherosclerotic plaque with a non-occlusive coronary artery thrombus can could be wht
unstable angina pectoris
130
what exaccebrates symtooms of aortic stnosis
how do fatty streaks appear
whaich murmur is seen in mitral regurgtation and mitral regurg exaccebration
a fib and why
Fatty streaks appear macroscopically as flat yellow discolorations with irregular borders on the luminal surfaces of blood vessels, including the aorta. Sta
MR exaccebration axilla murmur not seen
131
continutity equation
his concept is expressed mathematically via the continuity equation: A1V1 = A2V2
132
HIT 1 vs HIT 2
Direct interaction between heparin and platelets (e.g., heparin directly induces platelet aggregation)
No antibodies involved (nonimmunologic)
Heparin and platelet factor 4 (PF4) form a complex → production of IgG antibodies against the heparin-PF4 complex → IgG antibody-heparin-PF4 immunocomplex binds on platelet surface → platelet activation and aggregation → consumption of platelets (thrombocytopenia) and arterial/venous thrombosis
133
cml vs pcv
tear drop cells
134
pathophys of splenomegaly in hairy cell, vs cml
135
pica is associated with
altered sense of smell
Pica is also associated with zinc deficiency, pregnancy, and psychiatric conditions, though its etiology is not entirely understoo
zinc deficiency
136
how does tyrosine kinae inhibtor work
It binds to the active site for ATP on the abnormal BCR-ABL tyrosine kinase (caused by the Philadelphia chromosome) and prevents the phosphorylation of tyrosine residues on the enzyme's substrates. In turn, this inhibits proliferation
137
what happens to people with sickle cell disease
which bleeding location is epitaxis correlated to
talk about oxygen changes in anemia
they develop functional asplenia
vwf disease
Dyspnea, tachycardia, and evidence of hyperdynamic circulation (e.g., loud S1/S2, systolic ejection murmur due to increased blood flow) are features of severe anemia. In patients with anemia, the arterial partial pressure of oxygen (PaO2), which reflects dissolved oxygen content, and the arterial hemoglobin oxygen saturation (SaO2) remain normal. However, the total arterial oxygen content (CaO2), which is given by the formula [1.34 x SaO2 x hemoglobin concentration] + [0.003 x PaO2])
138
how to diagnosie antiphosophlipid antibody
Lupus anticoagulant (LA): leads to a prolonged aPTT
## Footnote
Mixing study: The patient's plasma is mixed with normal plasma. If the prolonged aPTT is caused by a lack of clotting factors, the factors contained in the normal plasma will normalize the aPTT. In the presence of lupus anticoagulants, the aPTT will remain unchanged.
Dilute Russell viper venom test: Lupus anticoagulant interacts with Russell viper venom, which usually induces the formation of blood clots. As LA binds the venom, this effect is suppressed, resulting in a prolonged aPTT.
139
MOA of all trans retinoic acid
Retinoic acid binds its nuclear receptors to stimulate histone acetylation, which promotes gene expression that regulates the maturation and proliferation of granulocytes.
140
effect of bence jones protien on tubules what other causes of renal dysfucntion in MM
causes tubular atrophy(Bj) proteinincluding AL amyloidosis (usually presenting with nephrotic syndrome due to glomerular dysfunction) or hypercalcemia (causing nephrocalcinosis).
141
febrile non hemolytic reaction=
Serum antibodies directed against donor HLA antigens have been associated with febrile non-hemolytic transfusion reactions (FNHTRs), as the antibodies may bind to HLA antigens on residual donor leukocytes in blood products and possibly stimulate the release of inflammatory cytokines.
142
if a patient has hemoglobinuria and flank pain what would the patient have
intravasuclar hemolysis
143
name.2 different types of hemolytic reaction
cold agglutins associated with which disease
major and minor( a person with scd will develop alloimmunization which could result in transfusion reaction)
CLL,HEPC,mYoco penumo
144
allogenic vs autologus stem cell transplantation
145
anti b2 glycoprotein MOA
These antibodies inactivate anticoagulant proteins (e.g., protein C and protein S, antithrombin III) and activate platelets and vascular endothelium, thereby resulting in a hypercoagulable state with an increased risk of arterial and venous thrombi.
146
AML risk factors
downs, cml,and radiation
147
explain role of ribavirin in HCV treatment and MOA of adverse effect
. Ribavirin-induced hemolytic anemia results from the accumulation of phosphorylated forms of ribavirin within red blood cells; since RBCs lack dephosphorylating enzymes, ribavirin accumulates within cells, leading to hemolysis. Because of the advent of newer HCV medications, ribavirin is typically used as an adjunct in patients with refractory hepatitis C infection.
Binds to rna polymerase/prevents gmp synthesis
148
hypocellular bone marrow seen in
HAIRY cell leukemia and myelofibrosis
149
what is the cause of fractures in Multiple myeloma how to diagnose from ideny
how can they develop analgesic nephropathy
proliferation of cells in the bone marrow inhibtis synthesis of cells, causing pancytopenia and skelatal destruction
since cells grow it causes hypercalcemia, non funtincal antibodies forme
A test in which sulfosalicylic acid is added to urine to measure urine proteins.
150
how to differentiate between myxedema and lymphedema
fluid is protein rich/gag rich
the other is lipid rich protein rich
if neutrophilic rich, it would be due to inflammation
151
how to differentiate between alpha thalesemia and beta thealesmeia
HB a2 would be seen in beta thalesemia
152
what sort of infarction does sickle cell disease have
Transient synovitis is a common cause of self-limited hip pain and limping in children and is often preceded by upper respiratory tract infection. However, most patients with transient synovitis are slightly younger (\< 10 years), and this patient's underlying sickle cell disease makes a different diagnosis more likel
trabeculae bone infarction
153
hemophius influenza non tybale B
and staph aureus
patients who have cystic fibrosis, alcohol use disorder, a history of IV drug use, or an immunocompromised status
heam has milder infections compared to the rest
154
what is porphria cutane
155
beta thaleesamia mutation
intron and promotor
if intron splice site mutation if promoto =point mutation
156
breastfeeding jaundice vs breat failure jaundice
a person with herditary spherocytosis will have folic acid deficiency or b12 deficiency
Pathophysiology: insufficient breast milk intake → lack of calories and inadequate quantities of bowel movements to remove bilirubin from the body → ↑ enterohepatic circulation → increased reabsorption of bilirubin from the intestines → unconjugated hyperbilirubinemia
Clinical features: onset within 1 week
Treatment: increase breastfeeding sessions, rehydration
Breast milk jaundice [2]
Pathophysiology: increased concentration of β-glucuronidase in breast milk → ↑ deconjugation and reabsorption of bilirubin → persistence of physiologic jaundice with unconjugated hyperbilirubinemia
Clinical features: onset within 2 weeks after birth; lasts for 4–13 weeks
157
what. is the indication of celcoxib and why is it used in genetic disorder of glantzmann thrombasthenia
glanzmann thromboasthenia needs coz 1 for formationo f thromboxane a 2 which stimulates aggregation so if cox 1 inhibited coul be a problem
158
lack of nucleus in RBC
mitochondria syntehsizes what
globin is not synthesized
heme is not hindered
ferrocheleatase/aminoleuviniv acid
159
person with epidural mass on vertebra of beta thalesmeia
160
clotting factors mutation leads to venous thromboembolism
antiphospholipid syndrome leads to both venous and arterial thromboembolism
161
a person with g6pd deficinecy how are ribose 5 phosphate produced
R5P is produced by the enzymes transketolase and transaldolase using byproducts of glycolysis, namely, fructose-6-phosphate (F6P) and glyceraldehyde-3-phosphate (G3P). F6P is formed by isomerization of G6P and G3P is produced by transaldolase. Therefore, transaldolase is one of the essential enzymes for the production of R5P, and thus nucleotide synthesis, in patients with G6PD deficiency.
162
what does lipid a activate
how can ecoli cause tubovarian abscess
The lipid A component of endotoxin activates tissue factor, the complement system, and macrophages,probably due to bacteremia
163
why is leuprolide combined with flutamide intially ot treat prostate cancer
164
tolterodine B3 receptor relaxation
cockroft gault equation
165
why cant creatinine clearence be used to assess kidney function\>60
Because a significant GFR drop is required before serum creatinine increases, serum creatinine cannot be used to assess kidney function at a GFR of \> 60 mL/min/1.73m2. This is termed the “creatinine-blind” range.
166
which is a better indicatiro serum creatine vs creatine clearnece
1.23 for males and 1.04 for females
obviously kideny creatinine why?
because serum creatinie Serum creatinine levels do not start rising until the GFR is reduced by approx. 50%.
167
anti phospholipase a2 antibodies
Anti-phospholipase A2 receptor antibodies (anti-PLA2R antibodies) bind to PLA2R (an autoantigen in glomerular podocytes) and thereby form immune complexes that activate the complement system, leading to podocyte injury. [15]
168
diabetic nephropathy pathophys
Chronic hyperglycemia and hyperinsulinemia stimulate collagen and glycoprotein synthesis within the GBM and mesangial matrix (protein glycosylation). I
169
why ace inhibitors increase renal plasma flow
Simultaneously, renal plasma flow (RPF) is increased and filtration fraction (FF) is decreased. The underlying mechanism is inhibition of angiotensin II synthesis, causing dilation of the efferent arteriole. This increases RPF and reduces GFR due to a decrease in glomerular filtration pressure. Also, the FF is decreased because GFR is decreased and RPF is increased (FF = GFR / RPF).
170
why cant we give ace inhibotors in heart failure
albuminuria coorelates with future risk of what
In patients with a preexisting reduction in RPF (e.g. heart failure), initiation of ACE inhibitors may lead to acute kidney injury.
cardiovasuclar events
171
treat good pasture
where does the lower third of ureter lie
cyclophosphamide
below the cardinal ligament
The ureters lie below the ovarian arteries within the infundibulopelvic ligament and are also susceptible to injury during ovarian surgeries (e.g., oophorectomy).
172
horse shoe kideny is always
incidentl
173
why do we have hypovoluemia in rhabdomyolisis
third fluid spacing in damaged muscle could preciptate kidney injury release phosokinase andserum myoglobin could lead to pigment nephropahty
174
How rapid progressive GN impairs renal function
so the cresecent =finbrin plus proliferating cells, compresses the glomerulus therefore could cause anuria
extracpaillary cell rpoliferation displaces glomerulus
175
why you have vitamin d and thyroxine defciciency in nephrotic compare mcd vs other disorders
very high prtoein diet why not allowed in nephrotic
why they can develop heparin resistance
metabolic disturnbances in nephrtoic and their consequences
176
Git manifestations of APCKD
177
how do you differentiate between selective and nonselective proteinuria\
gitelman syndrome symotoms
wjhat causes mesangial expansion in diabetic kidney
selective proteinuria will be loss of negative charge
nonselective proteinuria will be loss of glomeular archeticture
selective proteinuria predominantly albumin
non selective will be mid prtoeins
chondrocalcinosis
178
which drugs preciptate in kideny
Drugs such as acyclovir, indinavir, methotrexate, and ciprofloxacin are poorly soluble in urine and can cause renal tubule obstruction due to drug precipitation, building up as crystals that cause AKI within days to a week. This patient has not been exposed to any drugs that commonly cause crystal-induced AKI and has been sympto
179
xanthaloma glomeularnephritis
A rare form of chronic pyelonephritis characterized by chronic destructive granuloma formation
Associated with Proteus mirabilis and Escherichia coli infections
Large, irregular, yellow-orange masses on gross examination of the kidney (may be mistaken for a true renal neoplasm)
Histology: granulomatous tissue with lipid-laden foamy macrophages and multinucleated giant cells
180
Moa of pyelopnephritis
bacteria attaches to tubule cells, release cytokine s thereofre makes it more permeable therefore polynuclear cells enter the urine
181
why we give low sodium diet in renal stones
High sodium levels ultimately cause an increase in urine output, which results in both dehydration and increased amounts of calcium excreted in the urine. This increases the risk of calcium phosphate stones or calcium oxalate stones formation. This patient would benefit from a low-sodium, not a high-sodium, d
182
injury to pelvic splanchic nerves can
decrese sensation of bladdder fullness therefore can lead to overflow incontinecne
183
role of citrate in stone formation
Citrate inhibits stone formation by forming a soluble complex with calcium in the renal tubule, which reduces the amount of free calcium in the urine to bind with oxalate or phosphate. Citrate excretion in the kidney is strongly influenced by pH (systemic, tubular, and intracellular). Alkalosis increases renal citrate excretion, whereas acidosis decreases it.
184
hyperuricoria in stone formation
Associated with decreased solubility of calcium oxalate.
185
mechanism of gynecomastia in spirnolactone
Spironolactone inhibits the binding of androgens to their receptors as well as the activity of enzymes involved in androgen synthesis (e.g., 17,20-desmolase, 17α-hydroxylase). It also increases the peripheral conversion of testosterone to estradiol and displaces estradiol from SHBG.
186
changes in gfr/ ff in prfuse diarrhea
Profuse diarrhea can quickly lead to severe dehydration and hypovolemia, which would present with hypotension, tachycardia, and possibly, loss of consciousness. Hypovolemia leads to decreased renal plasma flow (RPF), and subsequently, a reduction in glomerular filtration rate. However, hypovolemia also stimulates the renin-angiotensin-aldosterone system, which attempts to mitigate the decrease in GFR by constricting the efferent arteriole. Therefore, in hypovolemic patients, the percentage reduction in GFR is less than the percentage reduction in RPF. The net effect is an increase in the filtration fraction.
PHYSIOLOGY OF THE KIDNEY
187
where is creatinine synthesized
Creatine is synthesized from arginine and glycine in two steps in the kidneys and liver and is then transported to the muscle cells and phosphorylated intracellularly to creatine phosphate
188
ARPCKD
Mutation in PKHD1 gene on chromosome 6, the gene that encodes for fibrocystin, a protein involved in the maintenance of primary cilia of the renal collecting duct and biliary epithelial cells
189
causes of hyoreninism hypoadlostrenism
In acute glomerulonephritis, hyporeninism occurs as a result of volume expansion Due to damage to the juxtaglomerular apparatus(diabeties) heparin ace increase renin supppress aldoestrone
190
how aldoestrone inhibits formation of ammonia
intracellular alkalosis
191
pseudohypoaldoestrinism aldoestrone resitance what are the causes what is liddle syndrome,
type 1 /type2 could be caused by obstructive uropathy and analgesic nephropathy liddle syndrome is basically gain of functionm utation ( decreased ubiquintin degradation by proteasomes), causes pseudohyperaldoestrinsim
192
glucogonoma what causes erythema
Nutritional deficiencies (e.g., decreased amino acid levels) are thought to be the underlying pathomechanism for the development of the erythema.
193
acanthosis nigricans see where and pathophys
acromegaly, Elevated levels of insulin stimulate keratinocyte and dermal fibroblast proliferation via interaction with insulin-like growth factor 1, resulting in epidermal hyperplasia and plaque-like lesions, as seen in this patient. In addition,
194
pcos what is the main hypothesis of SHBG decrease and how it affects
An inverse relationship between insulin levels and SHBG production has been suggested.
195
features of de querivian thyroididtis
Painful, diffuse, firm goiter, jaw pain(swalling cough
196
what are symtoms of thyroid malignancy
Also, this patient does not have symptoms suggestive of a thyroid malignancy (e.g., thyroid swelling, cervical lymphadenopathy, vocal cord palsy).
197
spindle cells in kidney
Sheets of spindle cells in the kidney can be seen in patients with angiomyolipoma
198
HPL b cell hyperplasia
Human placental lactogen causes pancreatic beta-cell hyperplasia and leads to an increase in insulin (and C-peptide) secretion as well as maternal insulin resistance. This ensures adequate glucose availability for the fetus. If maternal pancreatic function does not overcome insulin resistance, patients can develop gestational diabetes. In response to increased serum glucose concentrations, fetal production of insulin increases, which leads to increased fetal growth (macrosomia) as seen in this case.
199
which sort of diabetic patients are at increased risk of fetal abnormalities
Infants born to mothers with pregestational diabetes, not gestational diabetes, are at risk for intrauterine growth restriction. Infants born to mothers with gestational diabetes are at increased risk for macrosomia due to the anabolic effects of high insulin levels.
200
effects of graves diseas and fiabeties on fetus
Untreated diabetes during pregnancy can have teratogenic effects, putting infants at increased risk for congenital malformations including hypertrophic cardiomyopathy and small left colon syndrome. They are not, however, at increased risk for omphalocele. Pregestational diabetes (but not gestational diabetes) puts infants at increased risk of caudal regression syndrome.
201
cns causes of galactorhhea
anything destroying the dopamine pathway in pitutary stalk or prolactinoma
202
hypocalcemia causes what ecg findings
QT prolongation is seen in hypocalcemia due to slower calcium influx during phase 2 of the myocardial action potential and lengthening of the ST segment, whereas the T wave remains unaffected. Hypoparathyroidism, caused by trauma during thyroidectomy or parathyroidectomy, is the most common cause of hypocalcemia. Other, less common causes include vitamin D deficiency, PTH resistance, increased phosphate binding (rhabdomyolysis or tumor lysis syndrome), and hypomagnesemia.
HYPOCALCEMIA
203
what would increase with use of levothyroxine
Levothyroxine is a synthetic form of T4, which is converted to reverse T3 (biologically inactive) and T3 (biologically active) by a deiodinase in the blood. Since an increase of reactants leads to an increase in products, rT3 would be expected to increase after several weeks of levothyroxine therapy. T3 and T4 negatively regulate the secretion of TRH from the hypothalamus and of TSH from the anterior pituitary.
204
which molevular mechanism is involved in follicular adenoma
PAX8-PPAR gamma gene rearrangement is involved in the pathogenesis of follicular thyroid adenoma and follicular thyroid cancer, the second most common type of thyroid cancer. Unlike benign thyroid adenomas, follicular thyroid cancer is more likely to cause early invasion of the thyroid capsule and vasculature, making it the most likely diagnosis here.
205
where do parafollicular cells of thyroid gland come from
ultimobrachial body sepcifically thyroid aalange
206
what is adiponectin
A hormone produced by adipose tissue. Modulates insulin sensitivity, enhances fatty acid breakdown and has anti-inflammatory effects. Inversely related to adiposity.
207
which diabetics drugs have delayed onset
tzds enhances transcription
208
differentiate between classic and nonclassic 21 hydroxylase deficiency which is more common what are the sumtoms
209
what happens to TOTAL calcium ions when you infuse phosphate in it
calcium exists in three forms there will be a decrease in free ion calcium but an increase in total calcium
210
what antidiabetics used in gestational diabeties
Metformin and glyburide can
211
mechanism of hyperuriciemia in vongireke disease
212
calcitonin effects
its main goal is to decrease serum calcium so it inhibtis osteoclasts number 1 calcitonin keeps it in the bone
213
why we use high glucorticoids in acute adrenal insufficiency but we need both glucorticoids and aldoestrone in chronic adrenal insfufficiency
214
how to differentiate partial diabeties insipdus from central diapdies insipidus
The degree of responsiveness to desmopressin allows partial DI to be differentiated from complete central DI: In partial central DI, urine osmolality increases by approximately 10%, while in complete central DI, urine osmolality increases by over 50%. This patient's urine osmolality increased from 310 to 355 mOsm/kg H2O, an approximate 15% increase, which is sufficient to diagnose partial central DI.
215
siabeties insipuds cental
production problem or secretion problem ADH is produced in the hypothalamus and secreted from the posterior pituitary gland. Defects in the synthesis or secretion of ADH, e.g., those caused by brain tumors (craniopharyngioma), neurosurgery, traumatic brain injury, pituitary ischemia (Sheehan syndrome), or infection (meningitis), can cause central DI.
216
CF of siadh
SIADH patients are usually euvolemic, normotensive, and have no edema
217
symtoms of pitutary apoplexy
Pituitary apoplexy is often caused by hemorrhage into the pituitary gland. Intracerebral bleeding increases intracranial pressure, causing sudden, severe headache. The hematoma compresses the oculomotor nerves, which lie adjacent to the pituitary, causing acute onset of double vision. The disruption of pituitary secretion and release of ACTH can cause severe hypotension, as seen in this patient. Hemorrhage into the pituitary gland usually occurs into a previously existing pituitary adenoma (e.g., prolactinoma), which explains this patient's history of amenorrhea, recurrent headaches, and bitemporal hemianopsia.
218
a pt comes with charcort bouchard aneursym autospy findings hsow glomeulasa hyperplasia what is the mechanism of death
219
which drugs are associated with aki(diabetic)
Because SGLT2 inhibitors are associated with acute kidney injury, patients taking these agents should undergo regular renal function testing, and their use is contraindicated in patients with severe renal impairment. Other adverse effects of SGLT2 inhibitors include weight loss and (orthostatic) hypotension.
ANTIDIABETIC DRUGS
220
which diabetic drug causes agranulocytosis
Agranulocytosis is a rare complication of first-generation sulfonylurea use (chlorpropamide, tolbutamide) via an unknown mechanism.
221
what are brown tumors and why is it brown bone changes in hypperpth
Consist of osteoclasts and hemosiderin (hemosiderin accumulates in bone cysts as a result of hemorrhage)
Subperiosteal thinning
Most commonly seen in primary hyperparathyroidism but can also occur in secondary hyperparathyroidism (↑ PTH → activation of osteoclasts)
222
how to differentiate between brachial cyst and thyroglossal cyst
braachial cyst does not arise after URTI, however thyroid cyst can enlarge after urti
223
what degrades thyroglobulin after endocytosis
Instead, they degrade the prohormone thyroglobulin into T4 and T3 after its endocytosis into thyr
224
what is not destryoed in sheehan syndrome
In contrast, the posterior pituitary gland is thought to receive its blood supply from a higher-pressure arterial system. Accordingly, the posterior pituitary gland hormones, including antidiuretic hormone and oxytocin, are not typically affected in patients with Sheehan syndrome.
225
types of MODY and complication
n contrast to other subtypes of MODY, patients with MODY type II are not at risk for micro- or macrovascular complications, despite mild fasting hyperglycemia and chronically elevated HbA1c.
DIABETES MELLITUS
226
talk about islet amyloidosis
The pancreatic proteolytic enzymes that convert proinsulin and proamylin into insulin and amylin are not able to keep up with the high levels of production, which leads to the accumulation of proamyli
227
humoral calcium of malignancy
These laboratory values are seen in humoral hypercalcemia of malignancy, which is caused by PTHrP secretion from solid tumors (most commonly renal cancer, bladder cancer, ovarian cancer, or squamous cell cancers of the head, neck, or lung). PTHrP can activate PTH receptors and increase bone resorption, renal calcium absorption and phosphate excretion, leading to severe hypercalcemia and hypophosphatemia. Hypercalcemia further suppresses the secretion of PTH, causing decreased serum PTH levels. Unlike PTH, PTHrP does not stimulate the hydroxylation of 25-dihydroxyvitamin D to 1,25-dihydroxyvitamin D.
228
hyperechogenic on ultrasound is seen in what cancer,what will papillary cancer always have
thyroid cancer typically papillary why psammoma bodies,papillary cancer will always have lymphatic spread
229
thyroid nodule when to do monitoring, when do you do thyroid scintigraphy
If TSH levels are normal or elevated, this patient should undergo regular monitoring in case the tumor grows to ≥ 1 cm, , we do a thyroid scintigraphy to evaluate the functional status of a nodule
230
what is pathogensis of antiphospholipid antibody and give clinical features of livedoreticularis
Antibodies form complexes with anticoagulant proteins, thereby inactivating them (e.g., protein C, protein S, antithrombin III)
Antibodies activate platelets and vascular endothelium
blood clots in capillaries leads to swelling net like appearnece of skin
