January 2021 Flashcards

Question

What eye findings on exam are characteristic of thalamic ICH?

Answer 1

Specific eye findings - deviation of both eyes to the nose (down and inward) - Unequal pupils - Absence of light reaction - Skew deviation (unusual ocular deviation (strabismus), wherein the eyes move upward (hypertropia), but in opposite directions) - Ispilateral horner syndrome - Absence of convergence - Paralysis of upward gaze - Retraction nystagmus (uncertain how this presents)

Answer 2

Pons Pontine stroke presents and progresses over minutes – deep coma and quadriplegia, locked in syndrome, decerebrate rigiditiy

Answer 3

``` Occipital HA - the one localized head ache to be worried about Vomiting Gait ataxia Vertigo/Dizziness **Dysarthria** **Dysphagia** ```

Answer 4

Don't F with Pontine/Cerebellar ICH's Pontine ICH Cerebellar ICH – compression of 4th ventricle Stupor and altered mental status -> NUS!!!

Answer 5

Penetrating arteries in specific parts of the brain – putamen, thalamus, cerebellum and pons – are especially sensitive to hypertension-induced vascular injury

Answer 6

Cerebral amyloid angiopathy Probably the most common cause of lobar hemorrhage in elderly

Answer 7

Urine drug for amphetamines/cocaine

Answer 8

Intracranial is the umbrella term involving SAH, intracerebral hemorrhages Intracerebral hemorrhages are intraparenchymal bleeds, such as lobar hemorrhages SAH is NOT intracerebral, but is intracranial

Answer 9

ALL of them - Ischemic stroke - Intracerebral hemorrhage SAH (due to rupture of pre-existing aneurysm)

Answer 10

50% intracerebral hemorrhages 50% SAH, hence a young person who presents with SAH may have underlying aneurysm and the addition of stimulants pushed him over the edge

Answer 11

ANY! But typically subdural and lobar hemorrhages

Answer 12

ANY! But typically subdural and lobar hemorrhages

Answer 13

Intraparenchymal hemorrhages in the temporal and inferior frontal lobes that will also involve the subarachnoid, subdural and epidural spaces

Answer 14

Choriocarcinoma Malignant melanoma RCC Bronchogenic carcinoma

Answer 15

Yes, strong recommendation E.g. if patient is on VKA, treat with Vit K and PCC (FFP is not available)

Answer 16

“Spot sign” which is an enhancement seen within the hematoma which is associated with increased risk of hematoma expansion, mortally and lower likelihood of functional recovery

Answer 17

Plt < 50,000

Answer 18

50-70 mmHg TIP: ½ of the goal BP 140 SBP

Answer 19

Causes vasoconstriction, hence decreases the perfusion and also the intracranial pressure Tip: think of hypoventilation, hypercarbia. Brain may interpret that has hypoxia, hence vasodilate, and hence lead to to increase ICP. Hyperventilation decreases CO2 and leads to the opposite

Answer 20

A tangle of vessels located across the cortex or deep within the brain substance. They are a shunt between arterial and venous systems made up of abnormally thin vessels that are mixture of artery/vein in nature.

Answer 21

Intracerebral hemorrhages that extend to subarachnoid spaces

Answer 22

Yes they are as well NUS consult! TIP: SAH = AVM treatment

Answer 23

``` Headache Seizure (30% of the case) ``` Clinical tip: unlike ICH from hypertension, which seizures are uncommon. In addition, ICH from hypertension presents more like a stroke syndrome

Answer 24

Patient with dural AV fistula has an arterial connection with venous sinus of the dural. If there is significant enough shunting of arterial blood flow to the venous system, that can cause ischemia. In addition, there can be venous hypertension from excessive flow, leading to SAH.

Answer 25

The rise and fall of voltage across a membrane that leads to a characteristic shape In regards to the cardiac cell, ions travelling through voltage-gated ion channels (aka current) produces the action potential

Answer 26

Action potentials are the rise and fall of voltages across a membrane that leads to a characteristic shape The voltage change from an action potential is the primary signal to trigger the intracellular release of Ca that leads to contraction

Answer 27

The function of many ion channels is both TIME and VOLTAGE dependent So, though an anti-arrhythmic may target only 1 ion channel, by altering the action potential shape and or duration, other ion channels are inevitably affected

Answer 28

Concentration gradients Electrical gradients

Answer 29

-90mV Meaning that the inside of the cell is -90mV relative to the outside Na K ATPase and fixed anionic charges within the cell help maintain this resting membrane potential

Answer 30

For K: - Electrical gradient: K wants to go into the cell since it’s negative - Concentration gradient: K wants to leave the cell since the concentration of K is greater within the cell compared to outside For Na: - Electrical gradient: Na wants to go into the cell since it’s negative Concentration gradient: Na wants to go into the cell since the concentration of Na is greater outside the cell compared to inside

Answer 31

Depolarization of a neighboring myocyte above a certain threshold potential triggers an action potential. The presence of gap junctions lead to the propagation of action potentials from cell to the next, cause neighboring cells to reach their threshold potential and trigger action potentials

Answer 32

TIP: The movement of each ion is easy to determine. All you have to do is remember whether the ion is predominantly intracellular or extracellular. In the case of Na (serum Na is 135-145), Na will enter into the cell during an action potential because is predominantly an extracellular ion. K – mostly intracellular – so will leave the cell Ca – EXCEPTION – will enter the cell Phase 0 – Na enters and depolarizes the cell Phase 1 – K leaves the cell via the “transient outward K channel” Phase 2 – (plateau) Ca enters the cell via the L type Ca channel/and at the end of phase 3, K leaves the cell again via delayed rectifier channel Phase 3 – K continues to leave the cell via the delayed rectifier cells

Answer 33

Basic concept: the action potentials produced by cells are dependent on the ion channels present on the cells. Hence, action potentials throughout the heart actually differ in morphology. AV node’s action potential is initiated inward current of Ca which is much smaller compared to the Na current of the atria Other way to think about it: the speed of an impulse is dependent on the magnitude of the current, the magnitude of the current is dependent on the number of available channels. Hence speed is directly related to channel

Answer 34

Obesity: BMI > 30 Hypoventilation: Day time hypercapnia Co2 > 45 Sleep disordered breathing (AKA OSA)

Answer 35

>90% of patients with OHS have OSA Actually 70% of patients with OHS have severe OSA (>30 AHI/hr) TIP: Think of OHS as OSA that is so bad that it has now spilled over into the day time. It is OSA 24/7

Answer 36

Simply 5 events/hour

Answer 37

PAP – Positive airway pressure PAP can refer to 3 different things - CPAP - BiPAP - PSV Watch out! Some, when speaking of NIV, mean Bipap and NOT CpAP

Answer 38

Basically the benefits of OSA and correction of daytime hypoxemia (PaO2>55) and hypercapnia

Answer 39

During sleep But the benefits are actually seen both in the night time AND day time!

Answer 40

Death In one study, 3 month follow up showed 10 to 25 % of patients discharged without PAP had died

Answer 41

Bipap upon admission Bipap upon discharge DIFFERENCE: CPAP is first line for chronic stable ambulatory patients

Answer 42

LANCET RCT Dec 2020 Already known to reduce rebleeding, but uncertain if that reduction in rebleeding actually leads to clinical outcomes 1 gm bolus, then 1 gm every 8 hours until after 24 hours or right before aneurysm treatment, which ever came first We enrolled 955 patients; 480 patients were randomly assigned to tranexamic acid and 475 patients to the control group. In the intention-to-treat analysis, good clinical outcome was observed in 287 (60%) of 475 patients in the tranexamic acid group, and 300 (64%) of 470 patients in the control group (treatment centre adjusted odds ratio 0·86, 95% CI 0·66-1·12) Conclusion: In patients with CT-proven subarachnoid haemorrhage, presumably caused by a ruptured aneurysm, ultra-early, short-term tranexamic acid treatment did not improve clinical outcome at 6 months, as measured by the modified Rankin Scale Post R, Germans MR, Tjerkstra MA, et al. Ultra-early tranexamic acid after subarachnoid haemorrhage (ULTRA): a randomised controlled trial. Lancet. 2020 Dec 21. pii: S0140-6736(20)32518-6. doi: 10.1016/S0140-6736(20)32518-6.

Answer 43

Genetic mutations are the most common cause, accounting for 50% to 60% of all cases

Answer 44

About 80% of inherited hearing loss by autosomal recessive transmission About 18% by autosomal dominant transmission and about 2% by X-linked recessive transmission

Answer 45

Hearing loss can be categorized by severity and type. Severity is defined by the threshold at which sound is heard. Mild = 25 to 40 dB. Moderate = 41 to 70 dB. Severe = 71 to 90 dB. Profound = greater than 90 dB.

Answer 46

Grade failure, even if mild hearing loss

Answer 47

Rule for identification of and intervention for congenital hearing loss Screening by 1 month Confirmation by 3 months Intervention by 6 months

Answer 48

It can occur at any location from the outer ear (pinna, external auditory canal) to the stapes footplate and oval window.

Answer 49

Inner ear (eg, the cochlea) and/or the auditory nerve (cranial nerve VIII).

Answer 50

The outer ear, comprising the auricle and external auditory canal (EAC) The middle ear, comprising the tympanic membrane, ossicles, and the middle ear space The inner ear, comprising the cochlea, semicircular canals, and internal auditory canals

Answer 51

CT is very sensitive for identifying acute hemorrhage and is considered the gold standard TIP: Makes sense since it is the first image for suspected ischemic stroke to rule out hemorrhage

Answer 52

HTN and anticoagulant therapy

Answer 53

Sites of bifurcations or branches of penetrating arteries, such as lenticulostriate, thalamus, brainstem, thus explaining the commons sites for ICH

Answer 54

Amyloid deposits in tunica media/adventitia of vessels, leading to increased fragility

Answer 55

- Older age - Lobar regions, especially the posterior areas of the brain - Multi-focal - Recurrent

Answer 56

- Early on, even within hours – NEUROLOGIC EMERGENCY! | - TIME IS BRAIN

Answer 57

SAH Unusual hematoma shape (non circular) Presence of edema out of proportion to the early time that ICH is first imaged Unusual location of hemorrhage Presence of a mass

Answer 58

Vitamin K PCC (if not, than FFP)

Answer 59

Vitamin K PCC (if not, than FFP)

Answer 60

Catheter is “tunneled” under the skin and “terminates” which, in IR terms, refers not to the catheter tip, but rather the exit site on the skin, away from the venous access site (that is, where the vein is punctured)

Answer 61

o With port – AKA a Port is a type of tunneled CVC | o Without port such as tunneled dialysis cathters

Answer 62

BOTH can be used for infusion, fluids, nutrition HD can ONLY be used in tunneled CVC WITHOUT port

Answer 63

o Internal jugular o Subclavian vein o Femoral o TIP: the same places a CVC in the ICU is placed

Answer 64

The right IJ leads to a short right brachiocephalic vein that leads to the SVC. However, the left IJ will lead to a long left brachiocephalic vein prior to ending in the SVC

Answer 65

o Severe, uncorrectable coagulopathy o Uncontrolled sepsis o Bacteremia

Answer 66

o Bleeding – bleeding o Air embolism -> shortness of breath/cardiovascular collapse o Pneumothorax -> shortness of breath o Wound dehiscence -> bleeding o Cather migration/malposition -> can grab chest x ray o Cardiac perforation -> chest pain/shortness of breath/arrhythmia o Infection ->

Answer 67

Cavoatrial junction

Answer 68

o Trendelenberg position o Left lateral decubitus o Aspiration through the CVC

Answer 69

Thrombosis and infection

Answer 70

In critically ill patients that have atrial fibrillation with rapid ventricular rate without pre-excitation In addn, it has been used for those with atrial fibrillation and heart failure as well (just like Digoxin) Beta blockers or NDCC may have hemodynamic effects that are detrimental to patients that are critically ill

Answer 71

Electric cardioversion (SYNCHONIZED) Clinical tip: Patient, s/p cardiac arrest and ROSC may have atrial fibrillation with rapid ventricular rate. Cardioversion could be an option

Answer 72

IV beta blockers and non-dihydopyridine calcium channel blockers (Diltiazem/Verapimil)

Answer 73

AV nodal ablation with permanent ventricular pacing is reasonable when pharmacological therapy is inadequate and rhythm control is not achievable

Answer 74

TIP: dosing of IV amiodarone in the acute setting depends on the indication – rate control vs rhythm control Rate control: Same as dead guy dose in ACLS 300mg IV over 1 hour, followed by 10-50mg/hour for the next 24 hours Rhythm control (AKA cardioversion): 150 mg IV over 10 minutes then 1 mg/min IV for 6 hours, then 0.5 mg/min IV for 18 hours or switch to oral therapy

Answer 75

NDCC Digoxin Amiodarone Beta blocker (from ESC) WHY: Basically anything that can block the AV node. Blocking the AV node encourages propagation via the bypass track, which unlike the AV node, doesn’t actually slow down impulses. Hence atrial fib down the bypass tract can lead to such high ventricular rates that it devolves into Vfib or Vtach According to the AHA 2014 guidelines. No mention of beta blockers

Answer 76

Patient’s with HF as it does NOT have a negative inotropic effect

Answer 77

Amiodarone could cardiovert someone, and if a patient is NOT on an anticoagulation, this could be devastating Digoxin is helpful when patients have underlying heart failure as it does not have a negative inotropic effect. So patients who present with HF and atrial fibrillation with rapid ventricular rate with soft pressures could benefit from Digoxin

Answer 78

BOTH supraventricular and ventricular though only FDA approved for ventricular arrhythmias Ex: Atrial fibrillation (or any other SVT) and ventricular arrhythmias Clinical tip: DOSING is the same! 150mg IV over 10 minutes, then 1 mg/min for 6 hours, then 0.5mg/min for 18 hours

Answer 79

Acute rate control in atrial fibrillation with rapid ventricular response Long term rate control (just like beta blocker/NDCC) Acute rhythm control (aka pharmacologic cardioversion) Long term maintenance of rhythm control (maintenance of NSR for atrial fibrillation such as after electrical cardioversion) TIP: It does everything!

Answer 80

Class III which is mainly characterized by blocking the K rectifier channel responsible for repolarization in the phase 3 part of action potential TIP: however, Amiodarone exhibits properties of all the other classes as well, that is, Na channel blockade, beta blockade and Ca channel blockade Tip: Salty banana (K and Iodine)

Answer 81

Class III which is mainly characterized by blocking the K rectifier channel responsible for repolarization in the phase 3 part of action potential Therefore it prolongs the action potential and the refractory period

Answer 82

THE SAME!!! 150 mg IV over 10 minutes then 1 mg/min IV for 6 hours, then 0.5 mg/min IV for 18 hours or switch to oral therapy

Answer 83

Ventricular arrhythmias – BOTH treatment and prophylaxis

Answer 84

BOTH bradyarrhythmias and tachyarrhythmias Bradyarrhythmias: bradycardia, AV blocks and IVCD’s which is why it is contraindicated in patients with 2nd and 3rd degree AV blocks and NO pacemakers AND avoided in patients with atrial fibrillation and pre-excitation Tachyarrhythmias: Can extend QRS and QTc; can lead to Torsades de pointes even with normal QTc BUT for IV formulation, NOT PO

Answer 85

The magnitude of the depolarizing current In the case of myocytes, that would mean Na channel availability since that determines Phase 0 In the case of AV node, Ca channel availability

Answer 86

The magnitude of the inward current, which occurs through the Ca channel in the AV nodal tissue, is much smaller compared to current generated by myocytes in which the Na channel is the means by which the inward current is created Lesson: The magnitude of the depolarizing current determines how fast an impulse is propagated

Answer 87

Open -> Inactivated -> Closed -> Open -> etc. Open state: Phase 0, during which time ions can flow across (aka current is produced) Inactivated state: In this state, Na channels can’t reopen until they reassume the closed state Closed state: during repolarizing, channel goes from inactivated to closed. It is during the closed state that the channel can again open

Answer 88

TIP: It’s all about channels Membrane potential determines amount of Na channels available (AKA voltage dependent) - Depolarized – less Na channels recovered from activated state - Repolarizing – more Na channels recovered from activated state - Resting membrane potential – most Na channels recovered from activated state Amount of Na channels available determines current Current determines action potential During the plateau phase of an action potential, there simply aren’t enough available Na channels. No Na channels, no currents. No currents, no action potentials

Answer 89

TIP: It’s all about channels

Answer 90

For a given membrane potential, there are less Na channels recovered from inactivated state

Answer 91

The longest period during which an extra stimulus fails to produce a propagated response This is a quantitative description of “refractoriness”

Answer 92

The ability for a cell, after depolarization, to not produce another action potential in the face of a stimulus TIP: Again, it’s all about the channels. The lack of sufficient Na channels is the basis of refractoriness. But not only sufficient channels, but sufficient channels that have RECOVERED from inactivated state

Answer 93

Na vs Ca channel Unrelated to timing vs timing Depolarization is largely controlled by Ca channels and the current produced by them in AV nodal tissue. Secondly, Ca channels have a slower recovery from inactivated state. So even if there are sufficient Ca channels available, they become ready for re-excitation only after a certain time. TLDR: Timing and Ca channels

Answer 94

1) Enhanced automaticity 2) Triggered automaticity 3) Reentry They can be interrelated, that is, a triggered automaticity may lead to renentry

Answer 95

Phase 4 For cells that have spontaneous diastolic depolarization, such as AV node and His purkinje cells, the slope of Phase 4 can be increased, leading to enhanced automaticity, basically increased rate

Answer 96

After depolarization is just as it sounds. It is an abnormal depolarization that occurs AFTER a normal action potential Triggered automaticity means that the after depolarization reaches a certain threshold and a second action potential is produced. This only occurs after a first normal action potential, the trigger

Answer 97

Delayed after depolarization means that the depolarization occurs late, specifically after full repolarization so occurs in phase 4. This is caused by Ca overload in the sarcoplasmic reticulum. Ca leaks into the cytosol. To get rid of Ca, it uses the Na-Ca exchanger, which brings Na inside the cell in exchange for Ca, thereby depolarizing the cell. Movement of Na into the cell creates a current Early after depolarization is when the after depolarization occurs early, specifically during phase 3. Multiple ion channels are attributed

Answer 98

Delayed after depolarization means that the depolarization occurs late, specifically after full repolarization so occurs in phase 4. This is caused by Ca overload in the sarcoplasmic reticulum. Ca leaks into the cytosol. To get rid of Ca, it uses the Na-Ca exchanger, which brings Na inside the cell in exchange for Ca, thereby depolarizing the cell. Movement of Na into the cell creates a current Early after depolarization is when the after depolarization occurs early, specifically during phase 3. Multiple ion channels are attributed

Answer 99

DADs occur more at rapid heart rates EADs occur more at slow heart rates (aka long action potential) which makes sense since the longer time you are in phase 3, the higher chance you have to having an EAD

Answer 100

EAD since polymorphic ventricular tachycardia is related to prolonged QT, hence long action potential

Answer 101

Normal circumstances: Sinus node propagates an impulse to both the AV node and the accessory pathway. It is the combination of ventricular activation through both these pathways that leads to the abnormal, prolonged, slurring QRS at NSR Reentry: At baseline, AV node and accessory pathway are characteristically different. Accessory pathway has longer refractory period AND lacks decremental conduction. (Def: the more frequently a tissue is stimulated, the slower it conducts) When a premature impulse is initiated and propagated, the accessory pathway is still refractory. Hence, it travels to the AV node, down the His Purkinje and by the time it reachs the accessory pathway, it is no longer refractory. Hence it goes to the atria, back to the AV node and on and on and on.

Answer 102

Yes! Like other consequences of chronic decompensated cirrhosis, HRS, like ascites, can occur in the acute setting of alcoholic hepatitis or acute liver failure

Answer 103

1) Increase of serum Cr by 0.3 within 48 hours 2) increase of serum creatinine by 50% (AKA 1.5 fold increase from baseline) within seven days Tip: guidelines also define acute kidney injury by urine output, but in the setting of cirrhosis is both difficult and impractical.

Answer 104

AKI: 2 or 7 days 1) Increase of serum Cr by 0.3 within 48 hours 2) increase of serum Creatinine by 50% (AKA 1.5 fold increase from baseline) within seven days AKD: < 3 mos - Cr increase <50% < 3 mos - GFR < 60 or GFR decrease for 35% or more < 3 mos CKD: >3 mos -GFR < 60 for > 3 mos Simply: AKI: 2 day or 7 days, purely by Cr AKD: <3 mos, by GFR or Cr CKD: >3 mos, purely by GFR

Answer 105

Overestimate Hence, underestimates the amount of kidney injury to have occurred

Answer 106

In some ways, it is kidney injury that occurs beyond the setting an AKI (2 days or within 7 day), but not beyond the setting that would signify CKD (>3 mos) It is the injury that precedes CKD

Answer 107

KDIGO 1) Increase of serum Cr by 0.3 within 48 hours 2) increase of serum creatinine by 50% (AKA 1.5 fold increase from baseline) within seven days

Answer 108

``` Stage I: the same definition as AKI per KDIGO, that is, absolute Cr > 0.3 or >50% increase - Stage1A: Cr<1.5 - Stage 1B: Cr > 1.5 Stage 2: Cr 2fold from baseline Stage 3: Cr 3 fold from baseline ```

Answer 109

Albumin 20%, 1g/kg daily for 2 days (max of 100g/day)

Answer 110

NGAL as it implies tubular damage

Answer 111

Combination of microcirculatory dysfunction and inflammation which looks at cirrhosis as not only a circulatory dysfunctional state, but also a pro-inflammatory state Inflammation from cytokines/chemokines which cause the upregulation of DAMPS and PAMPS which alter the function of the proximal tubules such that they prioritize survival over other functions such as NaCl absorption, so NaCl travel further down the nephon, leading to RAAS stimulation (interesting because in both the old and new theory of the pathophys of HRS, RAAS plays a role)

Answer 112

Vasocontrictors and albumin

Answer 113

Since the splanchnic vasodilation is a key step in the development of HRS, vasoconstrictors counteract that. Phys: Though portal hypertension implies a high amount of pressure in the portal system. Splanchnic vasodilation occurs as a consequence of NO that is excreted in response to the portal HTN. This leads not only to local vasodilation, but to systemic vasodilation. Hence, the kidney’s response is to RAAS. It is this localized hypoperfusion that the kidneys are damaged

Answer 114

20-40g/day

Answer 115

Until a complete response (that is, Scr < 1.5) or 14 days maximum

Answer 116

Terlipressin

Answer 117

If NOT Terlipressin + Albumin Norepinephrine + Albumin OR Midrodrine/Octreotide + Albumin

Answer 118

SCr within 0.3 of the baseline Cr

Answer 119

Improvement in stage of AKI (example, improvement from stage 2 AKI to Stage 1) but SCr still > 0.3 from baseline

Answer 120

Liver transplant

Answer 121

1) Anatomically defined circuit 2) Heterogeneity in the refractoriness among regions of the circuit 3) Slow conduction in one part of the circuit

Answer 122

By altering the 4 determinants of spontaneous pacemaker discharge 1) Increase maximum diastolic potential – aka hyperpolarize the cell so that the beginning of phase 4 starts at a more negative potential and so for the same given slope, it takes longer to reach the threshold potential that initiates an action potential. Overall, phase 4 is prolonged 2) Decrease phase 4 slope. This will lead to longer phase 4 to reach threshold potential. Phase 4 is prolonged 3) Increase threshold potential – means phase 4 has to reach a higher threshold prior to the initiation of an action potential. Overall phase 4 is prolonged 4) Increase action potential duration which basically prolongs phase 3

Answer 123

Adenosine and acetylcholine

Answer 124

Beta blockers

Answer 125

Blockade of Ca or Na channels

Answer 126

Blockade of K channels

Answer 127

1) Inhibit the inward current that is responsible for the upstroke – Block Na or Ca channels to prevent upstrokes Tip: all about the channels. No channels, no upstrokes 2) Inhibit afterdepolarizations

Answer 128

Blocking the action potential propagation – aka slowing the conduction In the case of WPW, blocking the AV node with beta blocker or CCB or adenosine will do the trick

Answer 129

Increase refractoriness. Slowing the conduction can lead to the development of reentrant arrhythmias and in the functionally defined circuits slowing conduction may only change the pathway and not extinguish the circuit

Answer 130

1) Block Na channels. This leads to less Na channels available to induce another impulse 2) Prolonging the action potential, whether by Na channels or any other means, will prolong refractory period a. Ex: Ca channel blockers in the SA/AV node b. Ex: blockers of the delayed rectifier currents (K channels in phase 3)

Answer 131

Ion channels undergo conformational change between 3 different states: closed, open and inactivated The ability of a drug to block an ion channel is dependent on the conformational state, that is, drugs will only have affinity to block ion channels in certain states. Na channel blockers only bind to ion channels in the “open” or “inactivated” state Hence, the efficacy of a drug to block a certain ion channel is dependent on the state of the ion channel, that is, “state dependent ion channel block” and factors that promote longer duration of time in those desired states

Answer 132

Inactivated and open states Hence, during each action potential, during the diastolic interval (phase 4), Na channel blockers dissociate and the block is released

Answer 133

Increased heart rate allows less time for Na channel blockers to dissociate – dissociation rate – so blocking is increased Lesson: dissociation rate determines efficacy of Na block

Answer 134

Ischemia is a state of depolarization. And in depolarized states, rate of recovery from block is slowed down. Hence, Na blocking efficacy is increased Rate of recovery refers to the rate at which an ion channel goes from open -> inactivated -> closed state Lesson: rate of recovery from block affects the efficacy of ion channel blockers

Answer 135

The QT interval is measured from the beginning of the QRS to the end of the T wave. It encompasses both depolarization and repolarization. ANY mechanisms that prolong the action potential duration can prolong the QT interval. This is often done by prolonging Phase 3, which is most commonly and foremost done by blocking the delayed potassium rectifier channel (IKr) Lesson: Malfunction of ion channels may lead to an intracellular excess of positively charged ions, i.e. either by an inadequate outflow of potassium ions or by an excessive inflow of sodium ions.The intracellular excess of positively charged ions prolongs ventricular repolarization and results in QT interval prolongation on the ECG. Hence the second way QT can be prolonged by drugs is by increase in the late Na current which slows intraventricular conduction

Answer 136

It’s all in the name – calcium channel blocker. It blocks Ca channels predominantly in the nodal tissues, such as SA/AV node. Slows conduction velocity and increases refractoriness

Answer 137

1) Extending the action potential: prolonging phase 3 or non-nodal cells with K channel blockers 2) Slowing conduction velocity: Calcium-channel blockers reduce the slope of phase 4 (referring to nodal tissue), thereby decreasing the rate of spontaneous depolarization, which reduces the rate of pacemaker firing. These drugs also decrease the slope of phase 0, which slows conduction velocity within the AV node. Overall, decreasing slope of 4 and 0 leads to slow conduction velocity, which leads to a longer ERP.

Answer 138

Malfunction of ion channels may lead to an intracellular excess of positively charged ions, i.e. either by an inadequate outflow of potassium ions or by an excessive inflow of sodium ions. The intracellular excess of positively charged ions prolongs ventricular repolarization and results in QT interval prolongation on the ECG. Hence the second way QT can be prolonged by drugs is by increase in the late Na current which slows intraventricular conduction Given the structural similarity between K+ and Na+ channels, it is possible that K+ channel blocking drugs also bind to Na channels

Answer 139

Pathology of the gastric mucosa due to portal hypertension that can lead to slow bleeding

Answer 140

Portal hypertension is a prerequisite for the development of portal hypertensive gastropathy (PHG). The pathogenesis of PHG may be related to both congestion and hyperemia in the stomach. This is supported by the finding that gastric mucosal blood flow is increased in patients with cirrhosis and PHG compared with those without PHG Because the gastric mucosa in the setting of PHG is friable, bleeding may occur when ectatic vessels rupture (though PHG is an uncommon cause of significant bleeding in patients with portal hypertension)

Answer 141

Snake like mosaic pattern that may be superimposed with red signs, a sign of severe PHG

Answer 142

GAVE is located in the gastric antrum, that is, the area before the pylorus. PHG is located at the opposite end, that is, the proximal stomach in the body and antrum In regards to appearance, GAVE is characterized by red spots WITHOUT a mosaic background

Answer 143

PHG and every form of enteropathy might be clinically important because they are sometimes responsible for insidious blood loss (chronic iron deficient anaemia) and in exceptional cases even overt acute bleeding.

Answer 144

NSBB and iron supplementation for chronic iron loss

Answer 145

Same is EVH as dictated by small uncontrolled studies Yes, that means: octreotide/PPI/Abx ppx

Answer 146

GOV1 – esophageal varices extending below the cardia into the lesser curvature GOV2 – esophageal varices extending below the cardia and into the fundus - cardiofundal varices IGV 1 – isolated in the fundus IGV 2 – isolated anywhere other than the fundus

Answer 147

GOV 1 – makes up 75% of the cases

Answer 148

GOV 2 – cardiofundal varices

Answer 149

Splanchnic venous thrombosis

Answer 150

PHG Acute gastroesophageal hemorrhage of ANY type Makes sense because in all those situations, patient has underlying cirrhosis and from presentation alone, you can’t tell if it is EV vs the others. In regards to GOV1 and 2, they both are extensions of EV, so it makes sense to treat them the same

Answer 151

Both European and US guidelines agree that 10 mEQ/day is the maximum change US guidelines differ in that they adjust the limit for patients at “high risk” for ODS – no more than 8 mEQ/day

Answer 152

HTS 3% over 10 minutes in the US, over 20 minutes in the UK x3 as needed

Answer 153

In acute hyponatremia, neurologic symptoms arise from cerebral edema given the shift of fluid from the extravascular space to the intracellular space. HTS leads to increased tonicity of the extravascular space, causing fluid shifts from intracellular to extracellular

Answer 154

``` Postoperative period Exercise MDMA Haloperidol Thiazide diuretics Desmopressin Oxytocin IV Cyclophosphamide Transurethral or hysteroscopic use of irrigants such as glycine, sorbitol or mannitol which can be absorbed and cause fluid shifs ```

Answer 155

Severe symptoms regardless of acute or chronic

Answer 156

100ml HTS 3% over 10 minutes up to 3 times

Answer 157

< 48 hours

Answer 158

Urine Na < 30 Explanation: in hypovolemic and even hypervolemic hyponatremia (effective blood volume is low), the body will respond with Na retention

Answer 159

Fat – hypercholesteremia Protein – high protein concentration Glucose – hyperglycemia

Answer 160

Urine Na > 30 Urine Osm > 100 Remember, “I” means inappropriate. Hence, in the setting of hypoosmolality, what is appropriate is getting rid of free water (Urine Osm <100) and retaining Na (Urine Na < 30)

Answer 161

AFTER Urine Na and Urine Osm is evaluated Volume status is notoriously difficult to assess from a PE standpoint

Answer 162

FeUrea > 12% highly specific and sensitive

Answer 163

Acute or symptomatic? ``` Urine Osm > 100 Or Urine Osm < 100 - Urine osm < 100: appropriate o Low solute intake o Primary polydipsia o Beer potomania - Urine osm > 100: inappropriate o Eval Urine Na ``` Urine Na > 30 OR Urine Na < 30 - Urine <30: Na retention which indicates low effective blood volume (hypervolemia) or true hypovolemia - Urine > 30: o SIADH o Endocrine causes: Adrenal insuff, Hypothyroid Wasting syndrome: renal salt wasting or cerebral salt wasting

Answer 164

Cerebral edema and inability of the neurons to have adapted to the shift in fluid

Answer 165

Hypotonic fluids or Desmopressin

Answer 166

When limit for Na change in one day is surpassed >10 mEQ/day > 8 mEQ/day (if high risk for ODS)

Answer 167

According to the European guidelines, in acute symptomatic hyponatremia, there may not be a restricted limit! Crazy! In chronic, there is a limit – 10 meQ/day (8 meQ/day if high risk for ODS)

Answer 168

Free water restriction (1 L/day)

Answer 169

Reduced free water intake and increase free water renal excretion

Answer 170

Severe symptoms, regardless of whether the hyponatremia is acute or chronic

Answer 171

Urea causes osmotic diuresis and free water excretion

Answer 172

Urine Osm >100 | Urine Na > 30

January 2021 Flashcards

(203 cards)