USMLE Flashcards

(166 cards)

1
Q

If a patient has NSTEMI, should we give DAPT?

A

Only if he opts for ONLY medical mx, then we can give DAPT. If he will go for non-emergency coronary angiography, PGY12 inhibitors should be kept on hold until after the coronary angio, to decide if patient requires CABG or not, because if he does PGY12 is

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2
Q

How to differentiate between UA and NSTEMI?

A

A significant troponin rise in 6 to 12 hours

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3
Q

patient with cocaine toxicity and chest pain. now waht?

A

IV benzodiazapine
Aspirin
CCB + GTN

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4
Q

surgical dehiscence

A

complication of cardiac surgery due to separation of sternum

Clicking with chest movement

Surgical emergency for sternal fixation

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5
Q

vasospastic angina / Prinzmetal’s angina

A

Chest pain during rest / sleep
ST elevation in contiguous leads on ECG
coronary angiography- no obstruction
Tx- CCB (preventative) / SL GTN (abortive)

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6
Q

patient with infarction + < LVEF =

A

cardiac remodelling = increased risk of v fib

improved with:
ACE i
MRA
BB (metoprolol)

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7
Q

POST- MI medications

A

DAPT
BB
ACEi
MRA
Statin

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8
Q

indications for statin

A

Primary
- LDL > 190
- Age > 40 + DM
- 10 year atherosclerotic cardiac risk > 7.5-10%

Secondary
- ACS
- stable angina
- CVD
- Arterial revascularization

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9
Q

LV aneurysm post-MI can cause HF and MR and thrombus formation

How do we differentiate it from papillary muscle rupture though?

A

Persistent ST elevation and deep Q waves in SAME leads that was there initially during MI

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10
Q

Free wall LV rupture causes

A

Cardiac tamponade (triad)
PEA with possible junctional rhythm

Where as Ischemia would cause pulseless v tach or V fib

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11
Q

Angina tx

A

BB first line- reduced contractility and HR (DHP-CCB added to it- systemic dilatation)

NDHP-CCB alternative to BB- also reduce contractility and HR

Nitrates

Ranolazine- reduced myocardial calcium influx

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12
Q

Chest pain typical of MI

A

STEMI -> urgent repurfusion

ECG changes or elevated troponin -> medical mx -> non urgent coronary angiography

Negative findings -> serial ECG + trop
- +ve, refer to point 2
- -ve, stress testing

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13
Q

pleural effusion post CABD

A

Observation if:
- small-moderate
- early onset post surgery
- no resp symptoms

None of the above are met?
Diagnositc thoracocentesis

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14
Q

Vasospastic angina similar to

Classic angina similar to

A

reynaud’s phenomenon

Intermittent claudication

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15
Q

When to Suspect RVMI

A

Patient presents with inferior MI

AND has:

Hypotension

Clear lungs

Elevated jugular venous pressure (JVP)

These signs suggest RV involvement → get a right-sided ECG
V4R ST elevation

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16
Q

mediantitis

A

complicstion of CABG, a deep tissue infection
Imaging -> culture and abx -> drainage

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17
Q

Sudden cardiaic death of post MI complications:

  1. Cardiac tamponade
  2. LV aneurysm
A
  1. PEA / asystole
  2. V tachs
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18
Q

HHT

A

Autosomal dominant

  • Epistaxis
  • AVM (in brain -> hemorrhagic stroke, lungs -> paradoxical emboli, causing ischemic stroke, GI tract)
  • Telangiectasia on lips, tongue, fingers
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19
Q

Cavernous sinus thrombosis

A

Affects CN III IV V1 V2 VI

infection thrombosis following sinusitis or dental infection or cellulitis

staph aureus

Headache- worse on lying down
orbital pain
proptosis (protrusion)
chemosis (swelling)
loss of sensation of bilateral V1 / V2 dermatomes (forehead and nose)

Dx- MR venography
Tx- Ceftriaxone + Metronidazole / heparin / surgical drainage

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20
Q

lacunar stroke

A

A/W HTN

due to lipohyalonosis

  • contralateral pure motor hemiparesis
  • contralateral pure sensory hemiparesis
  • contralateral ataxic hemiparesis
    dysarthric-clumsy hand syndrome
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21
Q

PCT
Ascending loop of henle
DCT
CD

A

-zolamide + mannitol
Loop diuretics
Thiazide diuretics
MRA

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22
Q

giant cell arteritis

A

Jaw claudication
Headache over the temples
amaurosis fugax or permenant vision loss (due to AION)

Polymyalgia rheumatica (stiffness in neck - shoulder girdle - pelvic girdle)

Limb claudication
Angina pectoris / ACS

Constitutional sx (fever, wright loss, night sweats, fatigue)

dx- temporal artery biopsy + high ESR

Tx- High dose corticosteroids
THIS CAN CAUSE DRUG-INDUCED MYOPATHY, AFFECTING LOWER LIMBS MOSTLY (painless)

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23
Q

curtain falling over eye

A

amaurosis fugax (painless, transient < 10 min monocular vision loss)

causes include:
carotid atherosclerosis
cardioembolism
giant cell arteritis

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24
Q

isolated nerve palsies can indicate

A

aneurysm that has ruptures causing SAH

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25
carotid artery dissection
unilateral headache ipsilateral horner's syndrome ptosis + pupillary constriction
26
Visual field defects: 1. Lesion at optic nerve 2. Lesion at optic chiasim 3. Lesion at right optic tract 4. Lesion at left optic tract 5. Lesion at right superior optic radiation 6. Lesion at right inferior optic radiation 7. Lesion at left superior optic radiation 8. Lesion at left inferior optic radiation 9. Lesion at right inferior + superior optic radiation 10. Lesion at left inferior + superior optic radiation 11. Peripheral vision loss 12. Blind spot at central vision 13. Unable to recognise faces - PBI (parietal - baum's - inferior quadtrantinpoia) - TMS (temporal - meyer's - superior quadtrantinpoia)
1. Monocular (blind in one eye) 2. Bitemporal hemianopia - Loss of temporal (lateral) visual fields in both eyes - inferior chiasmal compression = pitutary adenoma) - superior chiasmal compression = craniopharyngioma, more in children) 3. Left homonymous hemianopia (Same side visual field loss in both eyes) 4. Right homonymous hemianopia 5. Left inferior homonymous quadrantanopia - Contralateral parietal lobe pathology 6. Left superior homonymous quadrantanopia - Contralateral temporal lobe pathology 7. Right inferior homonymous quadrantanopia - Contralateral parietal lobe pathology 8. Right superior homonymous quadrantanopia - Contralateral temporal lobe pathology 9. Left homonymous hemianopia 10. Right homonymous hemianopia 11. Tunnel vision (Glucoma / retinitis pigmentosa) 12. Scotoma (optic neuropathy) 13. Prosopagnosia
27
Steven johnson syndrome
reaction to medication that starts with flu-like symptoms, followed by a painful rash that spreads and blisters Medications: - Allopurinol - Anticonvulsants (phenytoin, phenobarbital, carbamazepine, lamotrigine)
28
Trigeminal neuralgia
pain syndrome characterised by severe unilateral electric like pain. The vast majority of cases are idiopathic but compression of the trigeminal roots by tumours or vascular problems Tx- carbamazepine
29
Benedikt syndrome
CN III palsy Medial leminscus (contralateral loss of proprioception and vibration) Artery involved: PCA
30
Weber syndrome
CN III (down and out) corticospinal tract (contralateral hemiparesis) corticobulbar tract (pseudobulbar palsy - UMN + exaggerated gag reflex + spastic tongue) Artery involved: PCA
31
Wallenberg (lateral medullary syndrome)
Ipsilateral horner's syndrome (miosis ptosis anhydrosis) Ipsilateral facial sensory loss of pain and temperature contralateral sensory loss of pain and temperature CN 9 + 10 (hoarseness + absent gag reflex etc) Nystagmus vertigo PICA
32
MCA stroke (usually embolic from carotid artery disease)
contralateral motor + sensory weakness in arm + face > legs Left side (parietal) - Aphasia - right homonymous hemianopia Right side (parietal) - Hemineglect
33
ACA Stroke
contralateral motor + sensory weakness in legs > arm + face Urinary incontinence
34
Lacunar stroke
A/W HTN Caused by lipohylainosis - Contralateral pure motor hemiparesis of face + arm + leg EQUALLY - Contralateral pure sensory hemiparesis of face + arm + leg EQUALLY - Contralateral ataxic hemiparesis - Dysarthic-clumsy hand syndrome
35
dejerine rousyy syndrome
post lacunar (thalamus) stroke chronic burning pain on the contralateral side
36
1. UMN involvement and signs 2. LMN involve and signs 3. Bulbar involve and signs
1. Brain to spinal cord (extensor plantars) Hyperreflexia Spastic Positive or upgoing babinski / extensor plantars Clonus 2. Spinal cord to muscles (absent ankle reflex) Hyporeflexia Flaccid Fasciculations Muscle atrophy Weakness Absent or downgoing babinski / flexor plantars 3. Cranial nerve IX to XII Dysarthria Dysphagia Tongue fasciculations Tongue atrophy Absent gag reflex
37
Overall diseases 1. Only UMN 2. Only LMN 3. Mixed
1. - PLS - MS - Hereditary Spastic Paraplegia (HSP) - Stroke 2. - GBS - MG - Diabetic neuropathy - SMA - PMA 3. - ALS - PBP - Subacute combined degeneration of the cord (vitamin b12 deficiency) - Frederich's ataxia - Taboparesis (syphilis) - Syringomyelia
38
PCA stroke (usually atherosclerosis from vertebral or basilar artery)
if occipital lobe - Contralateral homonymous hemianopia with macular sparing if thalamic lobe - contralateral sensory loss
39
Acute decompensated heart failure
Assess clinically: - resp failure? -> NIPPV (BIPAP) - cardiogenic shock? -> dobutamine / milrinone Improve sx: - IV diuretics (lasix) Investigation: - ECG - ECHO - Troponin
40
complication of aortic dissection involves insufficiency of which valve? if a patient has aortic dissection and it extends distally -> complications:
aortic vlave (AR) stroke (carotid artery) horners syndrome (carotid sympathetic plexus) AR (aortic root annulus) MI (coronary artery ostia) tamponade (pericardium) hemothorax (pleural cavity) Intestinal ischemia Renal infarction Lower extremity paralysis (spinal arteries)
41
Syncope
Cardiac - Arrhythmogenic - Cardiovascular (valvular HD, CAD, structural HD, PE, tamponade) Non cardiac - Reflex * vasovagal * situational * carotid sinus syndrome - Orthostatic * orthostatic hypotension (> 20 mmHg drop from standing and sitting) * POTS
42
neonatal HOCM in diabetic mothers
thick interventricular septum (due to increased deposition of glycogen and fat) small ventricle Tx- IV fluids + BB Spontaneous regression by age 1
43
Hypoplastic left heart syndrome
underdeveloped left ventricle Cyanosis ensues Tx- 1. prostagalndin 2. palliative surgery 3. cardiac transplant if mx is refractory to the first two
44
chronic venous insufficiency
lipodermatosclerosis (upside down champagne sign) Stasis dermatitis Skin ulcer on medial malleolus Telangiectasia / varicose veins Pitting edema Leg pain Tx- leg elevation, exercises, compression stockings If all fail, doppler to be done ABPI to r/o PVD
45
Arterial ulcers
PVD (6 p's) Punched out ulcer Dorsum of foot etc Doesnt bleed Worse on elevating foot, better with putting it down ABPI to diagnose
46
perivalcular abcess
suspected in patients who have IE and have: - Persisntent bacteremia - AV blocks - Aortic regurgitation (early diastolic murmur heard best during expiration v4 LSB) Dx- TOE Tx- surgery
47
AR secondary to valve disease AR secondary to aortic root disease
best hear on expiration in V4 left sternal border best hear on expiration in V2 right sternal border
48
IE causes stenosis or regurgitaiton?
regurgitaiton, which causes HF
49
Rheumatic fever
PASES FAPIL Major: Pan-carditis Arthritis (poly) Sydenham's chorea Erythema marginatum Subcutaneous nodules Minor: Fever Arthralgia PR prolongation Increased inflammatory markers Leukocytosis
50
Indications for surgery in IE
Persistent bacteremia Hard to treat pathogens (fungus, MDR) HF Extension of infection (abscess / AV blocks) Large vegetation > 1cm (increasing risk of infective emboli)
51
Coarctation of the aorta is a
congenital cardiovascular anomaly characterized by a narrowing of the aortic lumen, typically located just distal to the origin of the left subclavian artery at the site of the ductus arteriosus (see Image. Coarctation of the Aorta). This condition results in a significant obstruction in blood flow, leading to increased pressure proximal to the constriction and reduced distal perfusion. Coarctation of the aorta presents with a broad spectrum of clinical manifestations, ranging from asymptomatic hypertension to life-threatening heart failure in infancy. Complications including hypertension, left ventricular hypertrophy, aortic dissection, and intracranial hemorrhage In infancy, symptoms of CHF occur a few days after delivery, especially during feeding, due to closure of PDA
52
OSA
Production of catcehcolamines during apneic episodes Obese Systemic HTN Nocturnal awakening Daytime fatigue Loud snoring RHF (due to pulmonary HTN) Tx- CPAP
53
innocent murmurs
everything normal grade 1-2 intensity Venous hum- continuous murmur, best heard over infraclavicular area, decreases when supine Still murmur- systolic, best heard over LLSB, increases when supine Pulmonic flow murmur- systolic, best heard in the LUSB, may radiate to axilla
54
Renal artery stenosis
due to: - atherosclerosis (older population) - firomuscular dysplasia (younger population- women) Worsening AKI after initiation of ACEi Recurrent Flash Pulmonary Edema HTN Abdominal bruit
55
Chronic use of OCP can precipitate
HTN VTE
56
CPVT (catchecolinergic polymorphic ventricular tachycardia)
Sudden cardiac death Mutation in RYR2 receptor of myocardium
57
Sudden cardiac death conditions
CPVT HOCM ARVC Brugada syndrome Congenital long QT syndrome
58
Commotio Cordis
Sudden blunt chest trauma (e.g., baseball hit) Induces ventricular fibrillation without structural damage.
59
Autosomal dominant: Ehlers donlos syndrome Marfans syndrome Achondroplasia
- Easy bruising, poor healing Joint hypermobility- dislocation High arched palate Normal height COLA gene Tall with long extremities Joint hypermobility- dislocation Aortic root abnormalities FBN1 gene Short stature Joint hypermobility- dislocation fibroblast growth factor receptor 3
60
Hematomas
Epidural = trauma + lucid interval + middle meningeal artery and biconvex on ct Subdural = gradual onset of fluctuating consciousness + alcoholics / elderly / anticoagulated patients who had trauma days back + crescent-shaped on CT + bridging veins Subarachnoid = ruptured aneurysm + worst headache of their life Intracerebral = HTN + charcot bouchard anuerysm + amyloid elderly and AVM (HHT) in children Intraparenchymal = HTN + lenticulostriate arteries Cephalohematoma = neonate + does not cross sutures. Subgaleal = neonate + does cross sutures
61
In stroke patients due to infective cardioembolism from IE, anti-thrombolytics are contraindicated. why
high risk for hemorrhagic transformation
62
Hemorrhagic stroke
1. BP control (140-160 mmHg) 2. Reverse anticoagulation 3. Maintain normal ICP - Mannitol (normal Cr + stable) / hypertonic saline (AKI / CKD + unstable) - Head elevation at 30* - Sedation to reduce metabolic demands - CSF removal (external ventricular drain) - Decompressive craniectomy
63
When do we do surgical evacuation of hematoma?
When there is an evidence of impeding brain herniation: - large hematoma with midline shift - Raised ICP refractory to medical mx
64
Rhabdomyolysis
Causes: - crush injuries - strenuous exercise - seizure - collapse/coma - drugs - co-prescribed statins with macrolides or fibrates Features - AKI due to ATN - CK > 5x ULON - Hypocalcaemia - Hyperphosphatemia - Hyperkalaemia - lactic acidosis (if prolonged unconciousness) - Myoglobinuria: dark or reddish-brown colour Mx- Aggressive IV Fluid Resuscitation
65
risk factors for pediatric ischemic strokes
Cardiac: - Congential that causes paradoxical emboli (PFO) - Bacterial endocarditis Vascular: - Non-inflammatory: * arterial dissection - Inflammatory: * Takayasu arteritis / vasculitis * SLE Hematologic: - Sickle cell disease
66
ischemic stroke mx
for patients with ischemic stroke, eligibility for thrombolysis and thrombectomy is evaluated independently, as patients can be eligible for both, one, or neither Refer to word document
67
-ve superficial abdominal reflex on one side Scoliosis patient Chiari malformation
Get MRI spine Syringomyelia When a patient has chiari malformation, its a congenital abnormality which causes can part of the cerebellum to herniate through the foramen magnum, resulting in increased pressure in the spinal canal, which can cause the CSF to rupture through the spinal cord, and forms a fluid filled cavity known as syringomyelia
68
Subclavian steal syndrom
Narrowing of the subclavian artery just before vertebral artery branches (atherosclerosis / vasculitis / rib impingment) Left arm > right arm Sx: - > 15 mmHg difference in BP between both arms - Radio-radial delay - Arm claudication - Arm numbness and parasthesia - Vertebrobasilar artery insufficiency sx (vertigo, disequilibrium, ataxia, other CN palsy sx etc.) Dx: CT/MR angiography Tx: Lifestyle modification HTN, DM, DLP control Stent placement
69
Idiopathic inflammatory myopathies
SIGNS OF IIM - Symmetrical proximal muscle weakness - Elevated CK + aldolase + AST + ALT + myoglobin - Classic EMG findings - Classic muscle biopsy findings (GOLD STANDARD) TYPES OF IIM - Dermatomyositis (anti-Mi-2 abs) * signs of IIM + skin rash * heliotrope rash * gottron papules * shawl rash - Polymyositis * signs of IIM without characteristic features of others (diagnosis of exclusion) - Overlap myositis * signs of IIM + other autoimmune disorders - Antisynthetase syndrome (anti-Jo-1 abs) * Triad: ILD + arthritis + signs of IIM * reynaud's phenomenon + mechanics hand - Inclusion body myositis * signs of IIM + symmetric distal muscle weakness (finger flexors) + dysphagia - Immune-mediated necrotizing myopathy (anti-SRP abs) * Severe form of IIM * A/W statin use - Juvenile IIM * signs of IIM in < 18 y/o
70
psychogenic pseduosyncope
type of conversion disorder prolonged LOC recalls events during LOC normal findings
71
myocarditis can cause
DCM in all chambers and hypokinesia
72
Suspected AAA
Upper / lower abdominal, flank, back, groin pain Hemodynamically stable: - CT abdomen -> Medical optimization and repair Hemodynamically unstable - Abdominal US -> emergency repair
73
ichthyosis vulgaris
scaly dry skin on legs, chest, and abdomen Defect in FLG gene Worse during winter, better in summer Tx- long baths + keratolytics
74
Bullous pemphigoid
Autoantibody formation prodrome eczematous / urticarial like rash that then becomes pruritic tense bullae tx- topical steroids (clobetasol) oral steroid / oral doxycycline
75
dermatitis herpetiformis
GFD Dapsone PO
76
Lichen planus
flat purple papules with overlying white scribbles (wickham stria)
77
Basal CC
pearly nodule with telangiectasia Diagnosis: Biopsy (shave, punch , excisional) Tx Excision with 4 mm margin
78
nickel contact dermatitis
hyperpigmented lichenified plaque
79
Benign neonatal skin conditions
Milia Miliaria rubra (heat rash) Erythema toxicum neonatorum Neonatal pustular melanosis Neonatal cephalic pustilosis (acne)
80
thyroid storm
causes - low SVR (vasodilation) - High cardiac output (increased VR + increased HR) - High PCWP (due to impeding high-output HF, causing back up of fluid in lungs)
81
anaphylaxis diagnostic criteria
rapid onset of sx + 1 of the following: - Skin involvement + hypotension OR resp distress - 2 or more system involvment: * skin * cardio * resp * GI - Hypotension right after being exposed to the allergen
82
staphylococcal toxic shock syndrome
menstruating women who use tampons Anti-staphylococcal abx
83
edward syndrome (trisomy 18)
- Rocker bottom feet - Clenched overlapping fingers - low set ears + micrognathia + prominent occipit - Heart defects - kidney defects - weak hip abduction
84
antihypertensive meds in pregos
New Moms Hate Labour Nifedipine (2) Methyldopa (4) Hydralazine (3) Labetalol (1)
85
TFT should be tested before starting statins
hypothyroidism-associated DLP needs to be treated with levothyroxine, because statins can cause statin myopathy
86
Thyroid storm
Surgery or childbirth or trauma High grade fever Tachycardia Hypertension A fib Lid lag Sweating delerium seizure Diarrhea Tx: - BB (Propanolol, esmolol if CHF, NDHP-CCB if asthma / reynaud's, or any other contraindication) (reduce adrenergic manifestations) - PTU (reduce hormone synthesis) - iodine solution (SSKI) (reduce thyroid hormone release) - Hydrocortisone (reduce conversion of t4 -> t3)
87
1. Malignant hyperthermia 2. Neuroleptic malignant syndrome 3. Serotonin syndrome
1. Anesthesia / succinylcholine / hyperthermia / hyperkalemia / hypercalcemia / high CK / rigidity / myoglobinuria / dantrolene / 2. antipsychotics (haloperidol / resperidone) or antiemetics (metoclopramide) / hyperthermia / hyperkalemia / hypocalcemia / lead-pipe rigidity / high CK / myoglobinuria / dantrolene + bromocriptine (dopamine agonist) 3. SSRI / SNRI / TCA / opioid / hyperthermia / hyperreflexia / rigidity / altered mental status / clonus / mydriasis / high CK / symptoms resolve within 24 hours of cessation of serotonergic drugs / benzodiazipine for agitation / cyprohepatidine
88
prego and thyroid
during first trimester bhcg stimulates tsh receptros to release t4 bhcg suppreses tsh
89
euthyrooid sick syndrome
occurs in severe non-thyroid illness Total + free t3 reduced reversed t3 elevated TSH + T4 normal (can be reduced if prolonged sickness)
90
pregnant mothers with graves disease (diagnosed or undiagnpsed)
causes neonatal thyrotoxicosis due to maternal passage of TSH stimulating abs Storm sx + goiter + low birth weight + microcephaly Methemazole + BB, for a few months, then D/C as it self resolves
91
subclinical hypotyrodism subclinical hyperthyroidism
high TSH / normal T3 + T4 low TSH / normal T3 + T4
92
93
absent superficial abdominal reflex scoliosis patient chairi malformation
get MRI spine to r/o syringomyelia its a fluid filled cavity in the spinal cord that occurs when a patient has increase in the CSF pressure Chairi malformation does that as it is a congenital defect that causes part of the cerebellum to herniate through the foramen magnum
94
when a hypothyroid mother is prego, what do we do with the levo dose when there is tx with glucocorticoid
increase it to meet demands since bhcg reduced tsh reduce dose of levo
95
Things that increase TBG
in return it increases total T4 OCP HRT Pregnancy
96
levothyroxine and biotin
if patietns are on biotin, they need to stop it for 3 - 7 days before blood withdrawel, as it can mimic hyperthyroidism For patients who are hypothyroid, it can make it seem like the dose of levo is OVER correcting them Also omeprazole and calcium salts reduce absorption of levo
97
Hyperparathyroidism
Primary - Due to PT adenoma (most common) -> hyperplasia -> carcinoma - PTH is high, calcium is high - Surgery - medical mx- bisphosphonates (if osteoporosis) / calcimimetics Secondary - Due to hypocalcemia, in return causes PTH hyperplasia * CKD * vitamin D deficiency * malabsorption: celiac's + IBD + bariatric surgery * Phenytoin + Rifampin + Denosumab - PTH is high, calcium is normal / low, phosphate is low (unless in CKD, it will be high) - treat underlying cause Tertiary - refractory PTH release in response to untreated sHPT - PTH is high, calcium is V. high - tx is like pHPT
98
Pseudohypoparathyroidism type 1A (PHP1A)
Autosomal dominant Inherited from the mother (GNAS gene imprinting) short stature intellectual disability Persistent hypocalcemia despite ↑ PTH levels
99
most common hormone released in pituatary adenoma
prolactinoma dopamine antagonst (bromocriptine)
100
dopamine (released from hypothalamus) inhibits
prolactin (released from pituatary)
101
Hyperprolactinemia
causes: - Pituitary adenoma (had headache and bitemporal hemianopsia) - Hypothalamic-pituitary stalk damage (less dopamine to inhibit prolactin) - Primary hypothyroidism (causes increased TRH which stimulates prolactin release) - Dopamine antagonists (antipsychotics) sx: inhibits GnRH -> less LH and FSH -> reduced estrogen, leading to: osteoporosis vaginal atrophy and dryness Galactorrhea low libido infertility due to anovulation amenorrhea dx: ↑ Serum prolactin > 20 ng/mL in men > 25 ng/mL in women tx: dopamine agonists (Cabergoline / bromocriptine)
102
Acromegaly Gigantism GH deficiency
Acromegaly: Excess GH + IGF-1 in adults Large hands, feet, coarse facial features, macroglossia, enlarged organs Dx: IGF-1 levels OGTT and check GH levels 2 hrs after, if not suppressed, it goes with acromegaly Tx Transsphenoidal adenomectomy Somatostatin analogs (octreotide) Gigantism: Excess GH + IGF-1 in kids (before epiphyseal plate closure) - IGF-1 level: typically ↓; may be normal - Confirmatory testing: GH stimulation test - Procedure *Record baseline serum GH level. Administer stimulating agent (e.g., macimorelin). * Interpretation: ↓ GH level supports a GH deficiency
103
causes of hyponatremia
SIADH (high urine osmolality) Hypovelmia (includes diuretic use) Adrenal insufficiency Hypothyroidism Polydipsia Hyperglycemia
104
SIADH
- Increased pituitary ADH secretion * stroke * trauma * infection - Paraneoplastic ectopic ADH production * small cell lung carcinoma - Nephrogenic SIADH * enhanced ADH receptor activation in the kidneys as a result of mutation of vasopressin-2 receptor gene sx: Euvolemic Hypoosmolarity Hyponatremia High urine sodium High urine osmolality tx: hypertonic saline
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AVP
AVP-D: Causes - Hereditary - Brain tumor - Neurosurgery - Hypopituitarism AVP-R: - Demeclocycline - Lithium - Hypokalemia - Hypercalcemia - ADPKD NOCTURIA (daytime sleepiness) Polyuria Polydipsia Dx: 24 hour urine collection (has to be > 3L) Urine osmolality <300? -> plasma sodium < 145? -> water deprivation test to distinguish between AVP and PP (if Na > 145 and plasma osmolality > 295, then no need to do WDT as AVP is confirmed) water deprivation test interpretation: - Urine osmolality increases to > 800 mOsm/kg: Primary polydipsia is confirmed. - Urine osmolality remains ≤ 800 mOsm/kg: AVP disorders are likely - to distinguish between AVP-D & AVP-R, administer desmopressin. Interpretation: - Initial urine osmolality 300–800 mOsm/kg and: * Significant increase (≥ 10%) after desmopressin: partial AVP-D * No or minimal increase (< 10%) after desmopressin: primary polydipsia - Initial urine osmolality < 300 mOsm/kg and: * Significant increase (> 50%) after desmopressin: complete AVP-D * No or moderate increase (< 50%) after desmopressin: AVP-R Alternative: Plasma copeptin (reflects circulating AVP) Measure random plasma copeptin levels. ≥ 21.4 pmol/L: AVP-R is confirmed. < 21.4 pmol/L: hypertonic saline infusion test. * > 4.9 pmol/L: primary polydipsia * ≤ 4.9 pmol/L: AVP-D Tx: AVP-D: desmopressin AVP-R: Thiazide diuertics + NSAIDs + Amiloride (IF AVP-R caused by lithium and patient HAS TO continue on it)
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hypopituitarism cause
Causes: - nonsecretory pituitary macroadenoma (> 10 mm) - pituitary apoplexy - Sheehan syndrome - Post irradiation GH -> delayed growth Prolactin -> failure of lactation LH & FSH -> hypogonadotrophic hypogonadism TSH -> secondary hypothyroisidm ACTH -> secondary adrenal insufficiency ADH (panhypopituitarism) -> AVP-D
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myxedema coma
complication of hypothyroidism IV levothyroxine IV liothyronine IV hydrocortisone
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Asthma attack
O-SHIT-ME Oxygen Salbutamol Hydrocortisone Ipratropium Theophylline Magnesium sulphate Escalate to ICU
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CAH
21 hydroxylase deficiency (more androgens, less mineralo + glucocorticoid) - Hyponatremia + hypotension + hyperkalemia + hypoglycemia + metabolic acidosis - elevated 17-hydrxyprogesterone - Classical * salt-wasting type Early onset (neonatal period) signs of shock hypoglycemia females present with ambigous genitalia * simple virilizing type early onset No signs of shock Males have precoscious puberty Females present with ambigous genitalia - Non-classical late onset (late childhood - adulthood) No signs of shock precocious puberty females have irreguler menses Hirsuitism Acne tx: * mineralocorticoid (Fludicoritisone) * glucocorticoid (hydrocortisone / prednisone / dexamethasone) 17 hydroxylase deficiency (more mineralo + glucocorticoid, less androgens) hypernatremia + hypertension + hypokalemia + metabolic alkalosis + hyperglycemia males have female external genitalia females have delayed puberty tx: spironolactone + estrogen RT for females 11 hydroxylase deficiency (more mineralo + glucocorticoid, more androgens) - hypernatremia + hypertension + hypokalemia + metabolic alkalosis + hyperglycemia - males have normal genitalia, but precocious puberty - Females have external male genitalia
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primary hyperaldosteronism (conn's)
Systolic blood pressure > 140 mm Hg or diastolic > 90 mm Hg AND resistant to three-drug therapy Hypernatremia Hypokalemia metabolic alkalosis dx- screening test: > ARR > PAC < PRA confirmatory test - Oral sodium loading test Adrenal venous sampling - shows if its uni or bilateral Unilateral- laparoscopic unilateral adrenalectomy BL- spironolactone
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hypercortisolism (cushing's syndrome)
Exogenous Endogenous - primary (ACTH-independent) * Adrenal adenoma - secondary (ACTH dependent) * Cushing's disease (ACTH secreting pituatary adenoma) * Ectopic ACTH production Sx: hirsuitism thin skin proximal muscle weakness purple abdominal striae central obesity buffulo hump moon facies hyperglycemia and insulin resistence depression decreased libido irregular menses dx (2 out of the 3): - 24-hr urine free cortisol collection - low dose dexamethasone suppression test - late night salivary cortisol Once all positive, check serum ACTH levels to differentiate between primary and secondary cushings syndrome If ACTH is high, it means its secondary CS. Do CRH stimulation test OR desmopressin test to differentiate between cushing's disease (ACTH high after CRH or desmopressin) and ectopic ACTH production (ACTH normal/low after CRH or desmopressin) tx: Surgical: - Primary hypercortisolism: unilateral or bilateral laparoscopic or open adrenalectomy for adrenocortical tumors - Cushing disease: transsphenoidal hypophysectomy - Ectopic ACTH production: tumor resection Medical: - Primary hypercortisolism: * Mifepristone * Ketoconazole - secondary hypercortisolism: * cabergoline * pasireotide
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Adrenal insufficiency
Primary: - Autoimmune adrenalitis - Infectious adrenalitis (TB | CMV in AIDS | histoplasmosis) - Adrenal hemorrhage (DIC, neisseria meningiditis -> sepsis -> waterhouse fridrechson syndrome) - Adrenalectomy - Vitamin B5 deficiency - 21β-hydroxylase deficiency - drug-induced adrenal insufficiency (KPFR- ketoconazole | phenytoin | fluconazole | rifampin) - infilteration (malignancy | amyloidosis | haemochromatosis) Secondary: (conditions that decrease ACTH production) - Sudden discontinuation of prolonged glucocorticoid use - Hypopituitarism * nonsecretory pituitary macroadenoma (> 10 mm) * pituitary apoplexy * Sheehan syndrome Tertiary: (conditions that decrease CRH production) - Sudden discontinuation of prolonged glucocorticoid use Sx: Primary: features of hypoaldosteronism + hypocortisolism + hypoandrogenism + hyperpigmentation on non-sunlight exposed areas secondary + tertiary: features of hypocortisolism + hypoandrogenism Dx: - Make sure patient is not on any steroids before test * 24 hrs after the last dose of hydrocortisone * 48-72 hrs after the last dose of prednisolone * 1 week after the last dose of dexamethasone - Morning cortisol * low in all (pAI + sAI + tAI) - Morning ACTH * high in pAI * low in sAI + tAI) - ACTH stimulation test (cosyntropin test) * in pAI, no increase in cortisol * in sAI, increase in cortisol * in tAI, little to no increase in cortisol - < PAC / > PRA - < DHEA-S Tx: pAI- * mineralocorticoid (Fludicoritisone) * glucocorticoid (hydrocortisone / prednisone / dexamethasone) * androgens (over-the-counter DHEA- as needed)
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adrenal crisis
hyperkalemia metabolic acidosis hyponatremia hypotension hypoglycemia TX: Glucocorticoid mineralocorticoid IV fluids D50% IV
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Concentrated urine and > 3L urine over 24 hrs?
osmotic diuresis to urea or glucosuria
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low specific gravity < 1.006 means
dilute urine
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craniopharyngioma rathke cleft cyst (if big)
endocrinopathies low GH + FSH + LH + TSH + ADH + ACTH bitemporal hemianopsia Rathe cleft cyst though has no calcifications
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what worsens graves opthalmoplegia?
radio iodine ablation
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Phaechromocytoma
adrenal medullary metanephrine secreting tumour A/W: MEN 2A / 2B + VHL + NF-1 Sx: - Polycythemia (if secretes EPO) - Episodic HTN (triggered by palpation fn the tumor area + foods rich in tyramine like wine and cheese + surgery + anesthetic agents) - Diaphoresis - Throbbing headache - Palpitations - Weight loss - Hyperglycemia - MEN 2A: Medullary thyroid cancer and parathyroid hyperplasia - MEN 2B: Medullary thyroid cancer, oral/intestinal neuromas, and marfanoid habitus - NF1: Cutaneous neurofibromas, cafe-au-lait spots, and Lisch nodules - VHL: Renal cell carcinoma, hemangioblastoma Dx: - Increased serum metanephrine (supine) - 24-hr urinary metanephrine level - CT abdomen and pelvis with contrast Tx: - Adrenalectomy (no-touch technique) - Preoperative management (7-14 days before surgery) * BP target 90>x>130/80 mmHg Start with alpha blockers: - Phenoxybenzamine - doxazosin * Heart rate target 60–80/min while seated Add a beta blocker after effective alpha blockade - Metoprolol - propranolol * Consider the following for additional blood pressure control: - CCB - Metyrosine * Ensure high sodium and fluid intake to prevent postoperative hypotension - Post-operative Look out for primary adrenal insufficiency and treat accordingly
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Nonneoplastic-physiologic hypercortisolism / pseudo-cushing's syndrome
Due to: Alcoholics Major depressive disorder Anorexia Obesity Pregnancy Poorly managed DM How to differentiate between that and true Cushing's syndrome? - Dexa-CRH test + desmopressin stimulation test Dexa-CRH test in psuedo-cushings and normal people would be little to no increase in ACTH + cortisol, since the pituatary closed off because of dexa, so no more CRH can stimulate it. where as in cushing's disease, there is no negative feedback, so ACTH is always producing meaning dexa couldnt stop it, and so CRH can stimulate it and further drive ACTH + cortisol UP
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Milk-alkali syndrome
Cause: - excessive intake of calcium carbonate supplement for osteoporosis - excessive intake of antacids - High dose thiazide diuretics / ACEi / ARBs / NSAIDS Sx: - Boans, stones, groans, psychiatric understones - Polydipsia + polyuria Dx: - Hypercalcemia - Hypophosphatemia - Hypomagnesemia - Metabolic alkalosis - AKI - Low PTH Tx: - Stop agent - Rehydration - Loop diuretics
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thyroid cancer tx
1-2 cm nodule with no lymph node invasion -> partial thyroidectomy > 2 cm nodule and / or lymph node involvement -> total thyroidectomy Post surgery, to reduce recurrence: - Radioiodine ablation - Adequate doses of thyroid replacement to suppress TSH (stimulates growth of metastatic cells)
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phenylketonuria
autosomal recessive gene mutation (phenylalanine hydroxylase) that converts phenylalanine to tyrosine Sx: - Microcephaly - Developmental delay - Intellectual disability - Seizures - Hypopigmentation - Bad body odor - Eczema Dx: - High phenylalanine levels (serum amino acid analysis) Tx: - Phenylalanine restricted diet (protein rich) - Tyrosine supplements
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Causes of myopathy
IIM Hypothyroidism (+ myalgia + absent delayed reflexes) Cushings syndrome Corticosteroid Statin- (especially in combination with omeprazole or macrolide or fibrates)
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causes of hypercalcemia + low PTH
malignancy (PTHrP or increased 1,25-dihydroxyvitamin D) Immobilization Vitamin D toxicity Vitamin A toxicity Milk-alkali syndrome
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SIRS Sepsis Severe sepsis
> 2 from the following criteria: - Fever > 38 *C or < 36*C - HR > 90 - RR > 20 or PaCO2 < 32 - WBC > 12,000 or < 4,000 > 2 SIRS criteria + suspected or confirmed underlying infection Sepsis + at least 1 organ damage
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Osteoporosis tx
Bisphosphonates (alderonate) - Avoid in renal impairment Denosumab - Can cause hypocalcemia, skin reactions, and infections Raloxifene - Recommended for patients with increased risk of breast cancer - Increases risk of DVT
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humoral hypercalcemia of malignancy (HHM)
Hypercalecmia due to release of PTHrP by malignant cells Prevalant in: Squamous cell carcinoma (lung) Renal and bladder Ovarian and breast
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Hypercalcemia in malignancy causes
- PTHrP (HHM) - Bone metastasis / osteolytic malignancies (breast + MM) - Increased 1,25-dihydroxyvitamin D (hodgkin's lymphoma)
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Hypocalcemia Hypercalcemia
Hypoparathyroidism (low PTH) * Post-operative neck surgery * Autoimmune * Non-autoimmune destruction but infilterative (haemochromatosis | wilson) * DiGeorge syndrome * TSS Secondary hyperparathyoidism TLS Rhabdo Blood transfusion EDTA (used in lead poisoning) Hyperreflexia Seizures Pararsthesias Chvostek's sign (facial twitch with tapping) Trousseau's sign (carpal spasm with BP cuff) Bones, stones, groans, psychaitric undertones polyuria pancreaitits PUD
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TLS
Occurs after initiating cytotoxic treatment in patients with hematologic malignancies Hypocalcemia Hyperkalemia Hyperphosphatemia Hyperuricemia AKI (PUKE Calcium) Phosphortus | uric acid |potasssium elevated Tx: Aggressive fluid IV mx Fix electrolyte imbalances Treat hyperuricemia: - Low risk prophylaxis- allopurinol - intermediate - high risk prophylaxis / tx of established TLS: Rasburicase
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Precocious puberty
early secondary sexual characteristics development before the age of 8 years in girls and 9 years in boys: - Bone age radiograph A) advanced bone age (≥2 years ahead of the patient’s chronological age) - high LH -> central precocious puberty / gonadotropin-dependent precocious puberty (early activation of HPG axis: idiopathic | CNS tumor (MRI brain to be done)) - Low LH -> GnRH stimulation test -> * Low LH -> peripheral precocious puberty / gonadotropin-independent precocious puberty (gonadal or adrenal release of excess sex hormones: non-classical CAH | adrenal / gonadal tumors | Primary hypothyroidism) * High LH -> CPP B) normal bone age (early activation of adrenal androgens) - isolated breast development -> premature thelarche - isolated uterine bleeding -> premature menarche - isolated pubic hair development -> premature pubarche - pubic hair, acne, and/or adult-type body odor -> premature adrenarche (hepatoblastoma ONLY in males) CPP tx: GnRH agonist (e.g., leuprolide, goserelin) PPP tx: Tx of underlying cause
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strumi ovari
women > 40 y/o pelvic mass, ascites, or abdominal pain thyrotoxicosis No thyroid enlargment
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KDIGO (AKI)
1. serum creatinine (SC) 2. Urine output (UO) Stage 1 - SCr: * 1.5 - 1.9 x baseline with 7 days * Increase of 0.3 mg/dL | 26.5 μmol/L within 48 hrs - UO: * < 0.5 ml/kg/hr over 6 - 12 hours Stage 2 - SCr: * 2 - 2.9 x baseline - UO: * < 0.5 ml/kg/hr over ≥ 12 hours Stage 3 - SCr: * ≥ 3 x baseline * Increase to ≥ 4 mg/dL | ≥ 354 μmol/L - UO: * < 0.3 ml/kg/hr over ≥ 24 hours * ≥ 12 hours anuric - Need for RRT (dialysis) - In patients < 18 years of age: decrease in eGFR to < 35 mL/min/1.73 m2
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Dibaetic nephropathy
Intensive glycemic control - Target HbA1C <7 - SGLT2i Intensive BP control - Target BP < 130/80 - ACEi Lipid loweing Smoking cessation
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Hypoglycemia in patients without diabetes mellitus
Drugs: quinolones, quinine, beta blockers Sepsis/critical illness Severe hepatic failure Anorexia nervosa (depleted glycogen stores) Alcohol (usually with prolonged starvation) Adrenal insufficiency Insulinoma Non-insulinoma pancreatogenous hypoglycemia syndrome Surreptitious insulin or sulfonylurea use
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MEN syndrome
- MEN 1: Pituatary adenoma (prolactinoma) Parathyroid hyperplasia Pancreatic tumors (gastrinoma) - MEN 2A: Parathyroid hyperplasia Medullary thyroid cancer Phaechromocytoma - MEN 2B: Oral / intestinal neuromas Marfanoid habitus Medullary thyroid cancer Phaechromocytoma
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APS
Pro-thrombotic state Happens mostly with other AI diseases (SLE, RA) Miscarriages DVT PVD Thrombosis in organs Livedo reticularis Dx: Symptomatic + the presence of ≥ 1 type of aPL antibody supports the diagnosis: - Lupus anticoagulant - Anticardiolipin (IgG and IgM) - Anti-β2-glycoprotein antibodies (IgG and IgM) Asymptomatic + +ve aPL abs -> no diagnosis HOWEVER Further supportive factors to support the diagnosis: Positive antibodies against: Annexin Protein C Protein S ANA abs Anti-dsDNA antibodies *Patients with APS can test false positive for syphilis (positive VDRL or RPR) because the antigen used in syphilis tests is cardiolipin.* Tx: Non-pregnant patients: - High risk undiagnosed APS (asymptomatic + +ve aPL) -> Aspirin - Diagnosed APS -> warfarin Pregnant patients: - High risk undiagnosed APS (asymptomatic + +ve aPL) -> Aspirin - Diagnosed APS -> Aspirin + LMWH / UFH (theraputic in thrombosis, prophylactic if no thrombosis)
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Causes of recurrent pregnancy loss
Cervical insufficiency APS Celiac PCOS Hypothyroidism DM Hyperprolactinemia
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Subclinical hypothyroidism tx
can transform to overt hypothyroidism if not treated with regards to specific indications 1. TSH >10 mIU/L - Treat with levothyroxine (regardless of symptoms or age) 2. TSH 4.5–10 mIU/L Treat if: Age <65 and symptomatic (fatigue, depression, weight gain) +ve anti-TPO abs Pregnant or trying to conceive Presence of goiter Lipid abnormalities Cardiovascular risk factors
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When to do FNA for thyroid nodule
> 1 cm nodule with high risk sonographic features (internal vascularity + microcalcifications + irregular margins) > 2 cm nodule with no sonographic features
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pure breast milk diet without supplementation causes
vitamin D deficiency (rickets) Causes: Radial/ulnar bowing Skull bones that depress with pressure Delayed fontanel closure Widened wrists Lower extremity bowing (genu varum)
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1. Painless thyroiditis 2. Post partum thyroiditis 3. Subacute granulomatosis / de Quervain thyroiditis Cause Pain Phases Autoantibodies (TPO+) Radioactive Iodine Uptake Thyrotoxic Phase Recovery Treatment
1. Autoimmune Painless Hyperthyroid -> hypothyroid -> euthyroid Anti-TPO +ve Low radioactive iodine uptake There is a thyrotoxic phase Recovers in a year's time Propanolol if thyrotoxic sx / Levothyroxine if hypothyroid sx 2. Autoimmune (< 12 months postpartum) Painless Hyperthyroid -> hypothyroid -> euthyroid Anti-TPO +ve Low radioactive iodine uptake There is a thyrotoxic phase Recovers in a year's time Propanolol if thyrotoxic sx / Levothyroxine if hypothyroid sx 3. Post-viral inflammatory Painful Hyperthyroid -> hypothyroid -> euthyroid No antibodies Low radioactive iodine uptake There is a thyrotoxic phase Recovers in weeks to months Propanolol if thyrotoxic sx / Levothyroxine if hypothyroid sx
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Thyrotoxicosis in - low radioactive iodine uptake causes (thyroiditis) - high radioactive iodine uptake causes (Grave's, TMG)
- BB (Propanolol, esmolol if CHF, NDHP-CCB if asthma / reynaud's, or any other contraindication) - BB (Propanolol, esmolol if CHF, NDHP-CCB if asthma / reynaud's, or any other contraindication) (reduce adrenergic manifestations) - PTU / methimazole (reduce hormone synthesis) - iodine solution (SSKI) (reduce thyroid hormone release) - Hydrocortisone (reduce conversion of t4 -> t3) - Radioiodine ablation
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How does celiac cause secondary hyperparathyroidism
Celiac causes ADEK vitamins deficiency Vitamin D deficiency causes PTH to be released which causes increased calcium release from bone + increased renal reabsorption, and suppresses renal phosphate reabsorption -> normal - low calcium | low phosphate | high PTH
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wet beriberi
Thiamine deficiency High-output cardiac failure (due to systemic vasodilation) Dilated cardiomyopathy
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tricuspid atresia
central cyanosis absent tricuspid valve PS enlarged RA (p pulmonale) hypoplastic RV ASD VSD (holosystolic murmur) ECG: LAD CXR: decreased pulmonary vascular markings
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TAPVR
Pulmonary vein delivers oxygenated blood to RA instead of LA -> cyanosis RA + RV enlargement ECG: RAD CXR: Increased pulmonary vascular markings + cardiomegaly
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Truncus arteriosis
single arterial trunk arises from the heart and supplies the systemic + pulmonary circulations, instead of having separate aorta and pulmonary arteries -> cyanosis Systolic ejection murmur CXR: Increased pulmonary vascular markings + cardiomegaly
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Drug induced neutropenia
Methimazole / PTU Trimethoprim-sulfamethoxazole Clozapine Sulfasalazine Following sx occur within 3 months of initiating the drug: Fever Sore throat Oral ulcerations Tx: D/C culprit drug Abx if WBC < 1000
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MI with No Obstructive Coronary Arteries (MINOCA)
SCAD Vasospasm CO poisoning Takotsubo cardiomyopathy Coronary microvascular dysfunction (Impaired vasodilation and/or increased vasoconstriction of small coronary vessels)
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AAA screening
one time abdominal US for ages 65-75 who have: 1. smoking history 2. Family hx of ruptured AAA 3. male sex 4. HTN
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hemodynamic changes in the four major types of shock
CVP - PCWP - CO - SVR - SvO2 Cardiogenic (cold peripheries): ↑ ↑ ↓ ↑ ↓ Hypovolemic (cold peripheries): ↓ ↓ ↓ ↑ ↓ Obstructive (cold peripheries): PE / TP: ↑ ↓/↔ ↓ ↑ ↓ CT: ↑ ↑ ↓ ↑ ↓ Distributive (warm peripheries): Sepsis / anaphylaxis: ↓ ↓ ↑/↓ ↓ ↓/↑ Neurogenic: ↓ ↓ ↓ ↓ ↓
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Cushing's Triad
it is a classic clinical sign of increased intracranial pressure (ICP) and impending brain herniation Presents with: - Hypertension - Bradycardia - Irregular respirations
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What electrolyte imbalance is indicative of poor prognsis in HF patient?
Hyponatremia
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benzodiazipines in elderly
can worsen cognitive function, paradoxical agitation, increase falls
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benign murmurs
grade 1-2 intensity early or midsystolic decreases during standing / valsalva maneuvar asymptomatic patient
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Dementia ddx (neurodegenarative disorders):
Normal aging Pseudo-dementia Alzeheimers Vascular Lewy body Frontotemporal NPH Parkinsons Wernickie-korsakoff syndrome Wilson's disease Creutzfeldt-Jakob disease Huntington's disease Neurosyphilis Progressive multifocal leukoencephalopathy (e.g., in AIDS)
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Alzeheimer's
Clinical features: Cognitive impairement: - short term memory loss - temporal and spatial disorientation - language impairment - Impairment of executive functions and judgment Non-cognitive - apathy - agitation - depression Dx: DSM-5 for dementia criteria MRI brain: cerebral atrophy CSF: ↑ Phosphorylated-tau protein ↓ Aβ proteins Tx: AChEi (causes bradycardia, syncope, heart block): revastagmine | donepizil | galantamine NMDA receptor antagonist: memantine
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Pseudo-dementia
Depressed mood + dementia Patients are able to recall onset of symptoms Patient gives short answers, e.g., “I don't know"
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vascular dementia
causes: stroke with prolonged brain ischemia (LVO and / or lacunar infarcts) Comorbidities (DM DLP HTN AF) features of dementia + stroke sx depending on site Tx: treat underlying risk factors
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Frontotemporal dementia
Early changes in personality and behavior → inability to observe social etiquette Dx: DSM-5 for dementia criteria MRI brain: frontotemporal brain atrophy Pick bodies Tx: Supportive therapy
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Lewy body dementia
Parkinsonionsm (TRAP) Visual hallucinations Dementia Dx: MRI brain: atrophy of substantia innominata and mesopontine grey matter Lewy bodies: alpha-synuclein-positive Tx: Parkinsonian symptoms: Pharmacological treatment of parkinons Dementia symptoms: revastagmine | donepizil | galantamine | memantine Psychotic symptoms: In severe cases (e.g., functionally impairing psychosis), low-potency second-generation antipsychotic (e.g. quetiapine) can be administered. Can cause: Akinetic crisis- Characterized by inability to move, incomprehensible speech, and possibly hyperthermia Can also be caused by Abrupt withdrawal or reduction of dopaminergic meds in Parkinson’s patients
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NPH
Urinary incontinence Gait abnormalities (frequent falls, broad-based gait with short shuffling steps: gait apraxia) Dementia No signs of ICP MRI brain: Ventriculomegaly without sulcal enlargement Tx: VP shunt
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Parkinsons disease
Depletion of dopaminergic neurons in the substantia nigra Preclinical stage: - Mood disorders - Anosmia - Sleep disturbances (Excessive daytime sleepiness) - Constipation TRAP (unilateral onset): - Tremor (resting pill-rolling) - Rigidity (cogwheel) - Akinesia / bradykinesia - Postural instability (short shuffling steps) Tx: - Levodopa + carbidopa (Honeymoon period (end of dose akinesia)+ dyskinesia + avoid in glucoma as they increase IOP) - Anticholinergics: benztropine (urinary retention + avoid in glucoma as they increase IOP) - Nonergot dopamine receptor agonists: Ropinirole + Pramipexole (in younger patients who have levodopa induced dyskinesia) - NMDA antagonist: amantadine / memantine (akinetic crisis + Levodopa-induced dyskinesia) - COMT inhibitor: entacapone (used in combination with levodopa/carbidopa to improve end of dose akinesia) - MAO-B inhibitors: Selegiline (improve end of dose akinesia)
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Wernicke encephalopathy (acute, reversible) Korsakoff syndrome (chronic, irreversible)
Thiamine deficiency Chronic alcoholics - malabsorption - anorexia nervosa MRI brain: periventricular hemorrhage and/or atrophy of mammillary bodies Wernickie: AOC Ataxia (gait) - Occulomotor dysfunction (Gaze-induced horizontal/vertical nystagmus + Diplopia) - Confusion Tx: IV thiamine (FOLLOWED BY) glucose (NEVER THE OTHER WAY AROUND AS IT WORSENS ENCEPHALOPATHY) + alcohol abstinence Korsakoff: CARP Confobulation - Anterograde & Retrograde amnesia - Personality changes Tx: oral thiamine + alcohol abstinence
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