10⼀Heme-Onc/TOX I Flashcards

Question 1

Q

⬜ are 4 major triggers of vasooclusive crisis in Sickle Cell Disease patients

What is the treatment for vasooclusive crisis? (5)
_________________

Which med is used for long term management?

Answer

A

109DICK (Dehydration / Infection / Cold temp / [Kant breathe (hypoxia)])
_________________

acute tx = Rehydration / [abx and PAIN CONTROL (NSAID>opioids)] / heat / oxygen
_________________

chronic tx = Hydroxyurea

Question 2

Q

Which drugs cause Agranulocytosis? (6)

Answer

A

Gangs Can Certainly Crush Myeloblast & Promyelocytes

Ganciclovir

Clozapine

Carbamazepine

Colchicine

Methimazole(also Teratogenic–>Cutis Aplasia)

PTU

Question 3

Q

Victims of [smoke inhalation injury] should empircally be treated for Carbon Monoxide and what other chemical toxicity?

________________

What are the treatments for these toxicities? (4)

Answer

A

CYanide toxicity (➜ SEVERE lactic acidosis)

________________

“CYaMonoxide toxicity Needs Overt Smoke Help”

empiric tx for CYanide and ^(Carbon)Monoxide toxicity

[Nitrites (induces methemoglobinemia)]
Oxygen 100% (CO tx)
[Sodium thiosulfate]
HydroxoCobalamin (binds Cyanide ➜ excretable Cyanocobalamin)

_{{{CYanide is released from [burning PLASTIC] or [Nitroprusside_Rx]} | Tx = Hydroxocobalamin_{+/- Sodium thiosulfate}}}

Question 4

Q

Pulse Ox measures ⬜ which = ⬜

What does [PulseOx] read during methemoglobinemia?

________________

why?

Answer

A

**POSOSOP**
**P**ulse **O**x = **S**p**O**2 = [**S**aturation of **O**2 on **P**eripheralRBC]

* * *

**{low SpO2 < 85%}** = low **[**PulseOx SpO2_**RBC O2 Saturation**] \< 85%**}**

\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_

⚠️*NOTE*: Even though [PaO2 *oxygen partial pressure*] may read "normal", methemoglobin has lower affinity to O2 than Hgb = Mgb low binding to O2 ➜ **low [RBC O2 saturation]** = **{low POSOROS** = **[**PulseOx Sp*O2_**Saturation*] \< 85%**}**

\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_

*Dark chocolate colored blood*

## Footnote

[🔎SpO2 = Saturation of O2 in periphery/vein (via PulseOx)]
[ 🔎SaO2 = Saturation of O2 in **a**rtery (via ABG) = more accurate]

🫁**PaO2*ABG*** specifically refers to pressure solely exerted by dissolved oxygen in the arterial blood. It represents amount of oxygen actually dissolved in the plasma of arterial blood, rather than the amount that is bound to hemoglobin (which is reflected in measures like **SaO2*ABG*** or **SpO2*PulseOx***).

Question 5

Q

Dark chocolate colored blood = ⬜

________________

MOA for tx? (3)

Answer

A

Methemoglobinemia

________________

1st: [NADPH gives electron to [METHYLENE BLUE] ]
2nd: this converts [METHYLENE BLUE] –> [LeukoMethylene blue]
3rd: [LM reduces Methomoglobin –> back to Hgb]

Question 6

Q

s/s of [hypOcalcemia < 0.76 iCal] (7)

Answer

A

TQT + BOD + Chvostek
_________________
low calcium tx = IV CaGLUCONATE or CaChloride

Question 7

Q

SEVERE lead toxicity = [(⬜_{serum lead level}) or ⬜]

tx? (2)

Answer

A

≥70 ^{(or encephalopathy)}

Question 8

Q

Moderate lead toxicity = serum lead level of ⬜.

What’s unique about this level of toxicity ?

tx?

Answer

A

[Moderate lead toxicity = 45-69]

[XR lead lines from lead deposition on long bone metaphysis]

_________________

normal lead level = < 5

Question 9

Q

mild lead toxicity = serum lead level of ⬜

tx? (2)

Answer

A

5-44

tx = [no meds] and [repeat venous blood lead level in 1 month]
\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_

*normal lead level = \< 5*

Question 10

Q

Lead inhibits ⬜ which causes what effect on RBC?

major features of lead toxicity -10

Answer

A

[ferrochelatase and ALAD] ; [⬇︎heme synthesis and ⇪ RBC protoporphyrin]

\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_

**LL**\_**EE**\_**AA**\_**DD\_SS**

1-{**L**ead lines ([Burton's gingival lines] and on [metaphyses of long bones on xr]}

2-[A**L**AD and ferrochelatase] are inhibited by Lead

3-**E**ncephalopathy
4-**E**rythrocyte Basophilic Stippling (RBC retained rRNA aggregates due to Lead inhibiting rRNA degradation)
5-**A**bd colic
6-sideroblastic **A**nemia
7-**D**rops (wrist drop, foot drop, stocking glove)
8-[**D**imercaprol and EDTA are 1st line tx
9-***S**uc*cimer = peds tx ("it *Suc*ks to be a kid who ate lead")

10-**S**eventy-eight ⼀Houses older than 1978 have ⇪ for lead poisoning

## Footnote

*normal lead level < 5*

Question 11

Q

Iron deficiency is the most common pediatric nutritional deficiency and should be suspected in any child drinking greater than ⬜ cow’s milk /day

___________________

what is the order of physiological changes that occur after giving [ferrous sulfate] iron therapy?

Answer

A

>710 cc

_________________

[ferrous sulfate oral therapy] ➜ ([⇪ reticulocytes] ➜ [⇪ hct & hgb] ) by 1 mo

Question 12

Q

etx

Aplastic Crisis

Answer

A

AC = [AplasticCrisis)] = [Anemia in Sickle Cell pts,] 2/2 to parvoB19 replicating in (ProErythroblast_Erythroid precursors) → causes [⬇reticulocyte RBC] → [SEVERE ⬇︎Erythropoiesis _{= (⬇︎RBC/⬇︎Hgb)}] … in setting of already (sickle cell) anemic state = Crisis

{[anemia] from parvoB19} occurring in the presence of another (I.e. sickle cell) anemia = “Crisis” because RBC reserve will already be reduced from the other (sickle cell) anemia

Question 13

Q

What’s the difference between [Aplastic Crisis] and [Aplastic Anemia]?

Answer

A

AA = [(Aplastic Anemia)] =[All-cell PANcytopenia (including ⬇︎Erythropoiesis)] from [failure/destruction/suppression] of [Hematopoietic CD34 Myeloid Stem Cells] By [Bone Marrow T-cells^{( → hypOcellular bone marrow with fatty infiltration) = dry bone marrow tap}] … These [Bone Marrow T-cells] are activated by [IDIOPATHIC > Myelotoxic Drugs/Body Radiation/Virus/Fanconi)]

_________________

AC = [AplasticCrisis)] = [Anemia in Sickle Cell pts,] 2/2 to parvoB19 replicating in (ProErythroblast_Erythroid precursors) → causes [⬇reticulocyte RBC] → [SEVERE ⬇︎Erythropoiesis _{(⬇︎RBC/⬇︎Hgb)}] … in setting of already (sickle cell) anemic state = Crisis

[A C] from parvoB19 is worst in the presence of other anemias since RBC reserve will be reduced

Question 14

Q

cp for Radiation proctitis (4)

Answer

A

s/p pelvic radiation therapy
tenesmus
bloody diarrhea
[anal mucus discharge]

Question 15

Q

ITP

tx for Adults? (4)

[Immune Thrombocytopenic Purpura (ITP)

Answer

A

-obs^{(cutaneous sx}^but^{platelet≥30k )}

-[CTS | IVIG | antiD]^{(if bleeding | platelet< 30k)}

etx: Ab binds to platelet → both removed by Spleen macrophages → thrombocytopenia → purpura from uncontrolled bleeding

Question 16

Q

ITP

tx for peds? (4)

[Immune Thrombocytopenic Purpura (ITP)

Answer

A

-obs^{(if cutaneous sx only )}

-[CTS | IVIG | antiD]^{(if bleeding)}

etx: Ab binds to platelet → both removed by Spleen macrophages → thrombocytopenia → purpura from uncontrolled bleeding

Question 17

Q

MethanOL overdose antidote

Answer

A

Fomepizole
_________________

inhibits [hepatic alcohol dehydrogenase] from converting EG/methanol ➜ nephrotoxic metabolites

Question 18

Q

[Ethylene Glycol (antifreeze)] overdose antidote

Answer

A

Fomepizole
_________________

inhibits [hepatic alcohol dehydrogenase] from converting EG/methanol ➜ nephrotoxic metabolites

Question 19

Q

In a hemorrhaging patient, when do you transfuse [pRBC]? (2)
_________________

pRBC = packed RBC

Answer

A

hgb< 7

(or < 8 if CVD/CA)

Question 20

Q

What are the early sx of Sickle Cell disease ? (2)
_________________

how is this diagnosed?

Answer

A

-dactylitis (painful swelling of hands/feet 2/2 bone infarction)

-hemolytic anemia
\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_

Electrophoresis: {[Hgb **S**] with [NO Hgb **A**]}

Question 21

Q

Name the lab pair used to confrim SLE diagnosis

Answer

A

dana Smith

antidsDNA + anti-Smith

Question 22

Q

Hydoxychloroquine is a ⬜ used to treat what sx in SLE? (3)
_________________

How is CTS used in SLE patients? (2)

Answer

A

anti-malarial ;

Rash / Arthralgia / Soft tissue synovitis
_________________

acute SLE = low dose CTS

Chronic/SEVERE SLE = HIGH dose CTS

Question 23

Q

RA is a common cause of Anemia of Chronic Disease

How do you treat ACD 2/2 RA?

Answer

A

Infliximab_(AntiTNFα)

_{{ACD🔧: chronic/inflammation→ hepcidin→ [^{macrophage/intestinal}ferroportin]❌ from transfering Fe from FerriTin to Transferrin ➜ {[ ↧ Transferrin Saturation with paradoxic ⬇︎TIBC] , [↥ FerriTin],} and [⬇︎Fe_{**in circulation*}],}

Question 24

Q

Upregulators of Cytochrome P450 Enzymes (8)

Answer

A

Chronic alcoholics Steal Phen-Phen & Never Refuse Greasy Carbs which keeps them UP

Chronic alcohol use
St.John’s wort
Phenytoin
Phenobarbital
Nevirapine
Rifampin
Griseofulvin
Carbamazepine

Question 25

Q

Inhibitors of Cytochrome P450 Enzymes (11)

Answer

A

AAA RACKS In GQ Magazine

INHIBIT me from doing my job!

Acute Alcohol Abuse

Ritonavir (HIV Protease inhibitor)

Amiodarone

[Cimetidine & Ciprofloxacin]

Ketoconazole

Sulfonamides

[INH Isoniazid]

[Grapefruit Juice]

Quinidine

[Macrolides (except Azithro)]

Question 26

Q

What Substrates does Cytochrome P450 metabolize? (6)

Answer

A

Can Always Think When Outdoors, Son….i need it!

[Cyclosporine (Liver AND small intestine)]

AntiEpileptics

Theophylline

Warfarin

OCP

[Statins (NOT PRAVASTATIN)]

Question 27

Q

M.D. must recognize early signs of [Phenytoin toxicity > ⬜ mcg/ml]

What’s the earliest sign?

Answer

A

20

[Nystagmus on far lateral gaze]
_________________

other signs: [diplopia, ataxia ➜ coma]

[_Phenytoin10-(therapeutic)-20 < (TOXIC)]

Question 28

Q

Tx for Clostridium Botulinum poisoning - 3

Answer

A

[Equine Heptavalent Anti- Botulinum ^toxin _{(passive immunity)}]
[Ig Anti- Botulinum]
Guanidine

Question 29

Q

Jimson Weed Poisoning clinical presentation - 7

Answer

A

Jimson Weed = AntiCholinergic

“Blind as a bat, mad as a hatter, red as a beet, hot as a hare, dry as a bone, the bowel & bladder lose their tone, and the heart runs alone…..”

Blind as a bat = [Mydriasis and [cycloplegia (blurry vision especially when focusing on near objects)]
Mad as a hatter= Agitation & Hallucinations
Red as a Beet = Cutaneous flushing despite vasoconstriction
Hot as a hare = Hyperthermia from DEC ability to sweat
Dry as a bone= DEC Secretions (including sweat)
Bladder & Bowel lose tone
Heart runs alone = No vagal tone at SA –> Tachycardia

Question 30

Q

[MMalignant Hyperthermia] etx

Answer

A

After giving [inhaled anesthestics vs succinylcholine] to genetically predisposed (AUTO DOM) pts develop ➜

Malignant = Muscle Rigidity

Malignant = Malignant Unstable Vitals

Hyperthermia = Fever

Question 31

Q

MMalignant Hyperthermia Tx

Answer

A

Dantrolene

TREAT PROMPTLY! AS THIS IS LIFE THREATENING CONDITION!

Question 32

Q

TTP treatment

_________________

TTP = Thrombotic Thrombocytopenic Purpura

Answer

A

plasma EXCHANGE
_________________
_{(Tx = EXCHANGE plasma containing anti-A13vM or deficiency of A13vM for normal plasma)}

A13vM= [ADAMTS-13-vWF Metalloprotease])

_{TTP etx: [A13vM❌^{(or inhibition by shiga toxin in HUS)}] →uncontrolled vWF chain cleavage → widespread platelet traps/activation → thrombocytopenia + microagio hemolytic anemia → FMNRT TTP cp ^{⚠️TTP cp (aside from +Neuro and plasma EXCHANGE tx) = HUS cp}. ⼀ (TTP Tx = EXCHANGE plasma containing anti-A13vM or deficiency of A13vM for normal plasma)}

Question 33

Q

TTP MOD (4)

_________________

TTP = Thrombotic Thrombocytopenic Purpura

Answer

A

① {[A13vM (ADAMTS13_vWF Metalloprotease)] (responsible for degrading vWF Multimers)}

② A13vM❌ ^{= [acquired A13vM inhibition^{(by shiga toxin in HUS)}] or [ acquired A13vM deficiency] (2/2 CLOpidogrel | tiCLOpidine | cyCLOsporine | AIDS )}

③ ➜ allows ⇪ vWF Multimers to circulate and start cleaving large chains of von Willebrand factor from the vascular endothelium ➜ cleaved vWF ➜ widespread platelet traps and platelet activation ➜severe thrombocytopenia

④ +{RBC shearing ➜ [Schistocyte helmet cells], [INC Direct bilirubin], [microangiopathic hemolytic anemia]}

☞ TTP Symptom PENTAD (FMNRT)

_________________

tx = plasma EXCHANGE {(exchanges [anti-A13vM] and/or [low A13vM])for [more A13vM])}

_{💡in HUS, shiga toxin inhibits A13vM → similar TTP (but w/out neuro sx or plasma EXCHANGE tx) clinical presentation}

Question 34

Q

In RBC…

Adult Hemoglobin is made of 4 globin chains. What are they? fetal Hemoglobin?
_________________

βeta Thalassemia occurs because of ⬜ on Chromosome ⬜ of either parent. This → β-chain being ⬜

_________________

describe the 2 variants of βeta thalassemia

βeta Thalassemia = SEVERE anemia

Answer

A

_{hgbA_ADULT}[αα⼀αα / β⼀β] _{hgbF_fetal}[αα⼀αα / γ⼀γ]

[point mutations in splice & promoter sequences]; 11; [underproduced or ABSENT]

[αα⼀αα / ❌⼀β] = βT^minor(➜ β-chain underproduced= asx, [⇪ HgbA₂= dx], )

_________________

[αα⼀αα / ❌⼀❌] = βT^MAJOR(➜ β-chain ABSENT = early death , ⇪ HgbF|| temp tx = Hypertransfusion)
_________________

*αα (2 genes) = 1 α globin chain* | βT = βeta Thalassemia*
causes microcytic hypOchromic anemia*

Question 35

Q

In RBC…

[Adult Hemoglobin A] is made of 4 globin chains. What are they? fetal Hemoglobin?
_________________

αlpha thalassemia occurs due to ⬜ on chromosome ⬜. This can ultimately → 5 variants of hemoglobin makeup

Describe all 5 αT variants

alpha Thalassemiaa

Answer

A

_{hgbA_ADULT}[αα⼀αα / β⼀β] _{hgbF_fetal}[αα⼀αα / γ⼀γ]

[αlpha allele deletion (2 alleles per parent);] chromo 16

_________________
_I:[⬜α⼀αα / β⼀β] ➜ [αT⼀silent carrier]

_II:[⬜α⼀⬜α / β⼀β] ➜ [αT⼀trait^TRANS]

_II:[⬜⬜⼀αα / β⼀β] ➜ [αT⼀trait^{CIS(worst for offspring)}]

_III:[⬜⬜⼀⬜α / β⼀β] ➜ [αT⼀hb]

_IV:[⬜⬜⼀⬜⬜/ β⼀β] ➜ [αT⼀🅱🅶]

_________________
_________________

[αT⼀hb] = Hb(h)**tetramer of beta]

[αT⼀🅱🅶]= {[h🅱:T🅶 :HFD]} = {Hgb** 🅱ART tetramer of 🅶amma (Hydrops Fetalis^{(DIES IN UTERO)})**]}

*αα (2 genes) = 1 α globin chain* | αT = alpha Thalassemia

Question 36

Q

[Microcytic hypOchromic anemia] likely indicates the congenital hemolytic anemia ⬜.

Why are these patients at risk for organ damage 2/2 iron overload ? (3)

Answer

A

[Beta Thalassemia MAJOR [αα⼀αα / ❌⼀❌]] ;

Hypertransfusion tx overcomes effects of anemia and extramedullary hematopoiesis BUT also ➜ iron overload ➜ severe organ damage from iron deposition

Question 37

Q

[Anemia with Normal RDW] typically indicates ____

Answer

A

Thalassemia

Question 38

Q

What is Cooley Anemia?

________________

tx?

Answer

A

Beta thalassemia MAJOR (BOTH _{Mom and Dad} [chromo 11 β-globin genes] have [splice/promoter point mutations] →2 out of 2 ABSENT β-globin → [⇪ HgbF (a2g2)] = SEVERE COOLEY ANEMIA

________________

Tx = [chronic blood transfusion with deferadirox iron chelator]

Question 39

Q

DDx - 4

Answer

A

Target cells = HALT

HbC
Asplenia
Liver disease
Thalassemia (usually asx and REQUIRES NO TX if asx - occurs in Mediterranean people)

Question 40

Q

Dx

Answer

A

Thalassemia

image shows teardrop cells (Thalassemia also has Target cells)

Question 41

Q

What must you be VERY CAUTIOUS of when treating Megaloblastic macrocytic anemia with Vitamin B12?

Explain

Answer

A

hypOkalemia! (within 48h of VB12 tx)
_________________
VB12 supplement in moderate/Severe Megaloblastic macrocytic anemia will ➜ newly formed RBC ➜ RAPID INTRACELL UPTAKE OF K+ by new RBC ➜ hypOkalemia!

So…

[transfuse pRBC before VB12 ➜ blunts new RBC synthesis ➜ prevents hypOkalemia] + [monitor K+ 48h]

Question 42

Q

clinical presentation of neonatal polycythemia (5)

Answer

A

neonatal [PERIPHERAL venous hct > 65%]
**[ASX v 24h self limited] **
[+/- life threatening apnea]
[+/- hypOglycemia]
[+/- hyperviscosity (causes hypOperfusion ➜ lethargy, hypOtonia)]
_________________

1st hct comes from heel prick but = unreliable / confirmed by peripheral venous if abnml

Question 43

Q

treatment for neonatal polycythemia (3)

Answer

A

[HYDRATION]

2. CORRECT METABOLIC DERANGEMENT

–(if persist)–> [Partial exchange transfusion]

Question 44

Q

Patients with Multiple Myeloma need skeletal system assay for bone involvement

How is this done?

Answer

A

[Whole-Body-Cross-Sectional] eval with

[low-dose CT no contrast] > MRI or PET

Question 45

Q

What is hyperviscosity syndrome?

Answer

A

excessive production of monoclonal IgM (Waldenstrom Macroglobulinemia > Multiple Myeloma) ➜ congestion of brain’s microcirculation➜ [neuro ∆ /hearing ∆ /vision ∆]
_________________

neuro ∆ = somnolence/coma/HA

tx = plasmapheresis

Question 46

Q

There are several causes of Transiently elevated PSA, in which PSA should DEC by ⬜

What are the 3 causes of Persistently elevated PSA?

Answer

A

4-6 wks;

[CPCPPS]
BPH
Prostate CA
___________________________x____________________________________
^{(Chronic Prostatitis⼀Chronic Pelvic Pain Syndrome)}

Question 47

Q

What do patients use Ginkgo biloba for?
_________________

What’s the major potential side effect?

Answer

A

[“memory booster” (2/2 to its suggested propensity for ⇪ cerebral blood flow)]
_________________

Bleeding⁽^{inhibits platelet-activating factor + potentiates anticoagulants}⁾

(especially if combined with ASA/antiplatelet drugs)

“[herbs GSG] cause Bleeds”

Question 48

Q

Explain the relationship between [Tumor Lysis Syndrome] and Cardiac arrest (6)

Answer

A

Chemotherapy commonly ➜ {TLS = [⇪PUKED (and ⬇︎Ca+)]} –(if SEVERE hyperKalemia)–> [sine wave Wide QRS] ➜ VENTRICULAR ASYSTOLE ➜ CARDIAC ARREST

PUK = Phosphate/Uric acid/K+

Question 49

Q

FFP is used for what purpose? (2)

Answer

A

DIC
^{2nd line tx for}[Vitamin K deficiency coagulopathy^{(i.e. warfarin OD INR ≥2)}] ;

_{(2nd line tx for Warfarin OD because FFP requires large volume > 2L)}

Question 50

Q

When is Platelet transfusion indicated?

Answer

A

[platelet < 50K]

Question 51

Q

Laboratory findings for [Cobalamin VB12] deficiency (3)

Answer

A

PANcytopenia
Macrocytic anemia
low reticulocyte count

common cause of delirium/dementia in elderly!

Question 52

Q

Vegan Elderly patients p/w delirium or dementia should always make you c/f ⬜

Answer

A

[Cobalamin B12] deficiency!

Question 53

Q

Describe the 2 molecular reactions [Cobalamin B12] is responsible for

Question 54

Q

How does [Cobalamin VitB12] deficiency lead to hyperbilirubinemia

Answer

A

[Cobalamin VitB12 deficiency] ➜ defective DNA synthesis in bone marrow ➜ [Erythroid hyperplasia but with no maturation] = RBC megaloblastic transformation ➜ [intramedullary RBC hemolysis] ➜ [⇪ hemolysis markers ⼀indirect bilirubinemia, LDH, (low haptoglobin)] and no reticulocyte response

Question 55

Q

how do you emergently reverse Warfarin OD? (2)

Answer

A

[PCC +KIV] > ffp

_________________

PCC = Prothrombin Concentrate Complex (contain VitK factors and normalizes INR<10m) / KIV = Vitamin K IV(takes 12h to onset)*
ffp= fresh frozen plasma(2nd line due to large volume >2L required)*

Question 56

Q

These 3 agents emergently reverse ⬜

Briefly Describe each

a. [PCC ⼀ProThrombin Complex Concentrate]
b. [KIV ⼀Vitamin K IV]
c. [FFP ⼀Fresh Frozen Plasma]

Answer

A

WARFARIN

[PCC +KIV] > ffp

_________________

a. PCC = contain [VitK factors^2/7/9/10] and normalizes INR<10m
b. KIV = takes 12h to onset
c. ffp = 2nd line for warfarin reversal due to [large volume >2L required]

Question 57

Q

Warfarin

MOA

Question 58

Q

Treatment for Warfarin toxicity depends on INR and Bleeding

Name the [Warfarin toxicity] tx* (2) *for:

[^{(supratherapeutic)}INR: 3-4.5]

_with

[Bleeding: ≤minimal]

Answer

A

[Hold Warfarin x 1-2d] | [DEC dose]

Question 59

Q

Treatment for Warfarin toxicity depends on Bleeding and INR

Name the [Warfarin toxicity] tx* (2) *for:

[Bleeding: ≤minimal]

_with

[^{(supratherapeutic)}INR: 4.5-10]

Answer

A

Hold Warfarin ➜ Resume when INR therapeutic
[vitK_{Ld 1- 2.5mg} PO]^{(If INC risk of bleeding)}**

_________________

Question 60

Q

Treatment for Warfarin toxicity depends on INR and Bleeding

Name the [Warfarin toxicity] tx* (2) *for:

[^{(supratherapeutic)}INR: >10]

_with

[Bleeding: ≤minimal]

Answer

A

Hold Warfarin ➜ Resume when INR therapeutic
GIVE [vitK_HD_{2.5 - 5 mg} PO]

_________________

Question 61

Q

Treatment for Warfarin toxicity depends on INR and Bleeding

Name the [Warfarin toxicity] tx* (3) *for:

[INR: x]

_with

[Bleeding: SEVERE]

Answer

A

Hold Warfarin ➜ Resume when INR therapeutic
GIVE [vitK_UHD_{10 mg} IV]
GIVE [PCC]

_________________

Question 62

Q

What is Pernicious Anemia?

_________________

how is this diagnosed?

Answer

A

[Anti-ParietalCell and Anti-IntrinsicFactor] autoimmune destruction ➜ AMAG ➜ no IntrinsicFactor to facilitate {[Cobalamin VB12] terminal iLeum absorption} ➜ [mAcrocytic megaloblastic anemia]

dx = elevated Anti-IF

AMAG = Autoimmune Metaplastic Atrophic Gastritis

Question 63

Q

*HIGH YIELD*

Name the gastritis associated with pernicious anemia

_________________

What are the 3 main components of it’s MOD

Answer

A

AMAG = autoimmune destruction against intrinsic factor and oxyntic cells ➜ gastric fundus and gastric body destruction with:

glandular atrophy
intestinal metaplasia
intestinal inflammation

_________________

AMAG = Autoimmune Metaplastic Atrophic Gastritis

Question 64

Q

What is Tumor Lysis Syndrome? (5)

Answer

A

{[cytotoxic chemotherapy] or [high grade lymphoma]} ➜ rapid lysis of neoplastic cells ➜”pt PUKED”

Phosphate INC (⇪ [serum/urine P] binds [serum/urine Ca+] ➜ [⬇︎serum Ca+ and CaPhosphate renal stones])
{Uric acid INC from pUrine DNA bases (serum and [urine ➜ Uric Acid stones]) = (px=allopurinol and IVF)} = DIAGNOSIS
K+ INC ( ➜ arrhythmia)
[Elevated ^{(Ca+P & Uric Acid)}renal stones ➜ AKI (IVF px)]
[DNA base Purines] INC → Uric acid INC

Answer 63

A

[urate oxidase^{(not naturally in humans)} recombinant] = catalyzes conversion of [INC Uric acid^{(i.e. from Tumor Lysis Syndrome)}] ➜ [allantoin (excreted in urine)] for Tumor Lysis Syndrome px

_________________

Answer 64

A

Cancer = chemo ➜ [_TLSPUKED] ➜ [Elevated ^{(Ca+P & Uric Acid)}renal stones ➜ AKI]
Rasburicase only ⬇︎Uric Acid renal Stones. AKI can still be caused by Ca+P stones

Answer 65

A

[60% Head/Neck CA are locally advanced at time of dx = inoperable] ➜ CRT as a duo INC the 5 year survival rate

Answer 66

A

Violent PCP = [BENZO sedation]
Mild PCP = [low stimulation environment +/- benzo sedation]
***
[PCP (Phencyclidine)] is a [NMDA R Blocker hallucinogen]

Answer 67

A

physician should*
1. explain risks of herbal preparations
2. document that you counseled patient to avoid herbal prep
3. document patient refusal/response to avoid herbal prep
4. follow patient closely for adverse effects

Answer 68

A

PICC has [HIGHER UE DVT]

but…

PICC has lower

infections
procedural complications
patient discomfort

Answer 69

A

Total Iron Binding Capacity = TIBC = “Transferrin In Blood Calculation”

= [TOTAL amount of transferrin^{(transports iron)} in serum]

(by calculation)

Answer 70

A

_{{ACD🔧: chronic/inflammation→IL6 secretion → [hepatic hepcidin secretion]→ [^{macrophage/intestinal}ferroportin]❌ from transfering Fe from FerriTin to Transferrin ➜ {[ ↧ Transferrin Saturation _{with an accompanying Transferrin “activity pause” = stops Transferrin from scavenging blood for more Fe} → ⬇︎ Transferrin In Blood (⬇︎TIBC)] , [↥ FerriTin],} and _ultimately [⬇︎Fe_{**in circulation*}],}

Answer 71

A

⬇︎MCV

⬆︎Iron

Answer 72

A

[HgbBarts tetramer of gamma (Hydrops Fetalis)]

Intrauterine death 2/2 CHF

Answer 73

A

less severe variant of [Sickle Cell Disease_{(Hgb_SS & Hgb_SC)}]
➜ mild normocytic anemia
electrophoresis = [equal Hgb_S = Hgb_C]

Answer 74

A

[FerriTin < 15] = IDA

_________________

Most pts with [FerriTin 15-30] realistically are also iron deficient = Traditional rule can only rule IN IDA

Answer 75

A

[BorTezomib proteasome inhibitor]

OR

2.{[LD _{and if <70 yo}(➜ BMT)}

_{[Lenalidomide + Dexamethoasone] –> [Bone Marrow Transplant]}}

Answer 76

A

This does NOT automatically mean Multiple Myeloma. This can be seen in MGUS-Monoclonal Gammopathy of Unknown Significance which = common in older pts and only transforms to Multiple Myeloma 1%/year

Answer 77

A

Multiple Myeloma plasma cells overproduce IgM specifically –> hyperviscosity sx (HA, tinnitus)

Neuropathy
Engorged blood vessels
HA
tinnitus
Raynaud Phenomenon

Answer 78

A

PLASMAPHERESIS initially
Chlorambucil + Prednisone = long term OR
Fludarabine + Prednisone = long term

Answer 79

A

DDAVP desmopressin –(refractory)–> Factor 8 or vWF concentrate

_{DDAVP → ⇪Factor 8 → ⇪ vWF}

(DDAVP releases subendothelial stores of vWF)

Answer 80

A

CefTriaxone (Strep Pneumo)

+

Azithromycin (Mycoplasma PNA)

Answer 81

A

therapeutic phlebotomy

Answer 82

A

metastatic SQC

Answer 83

A

MELAS

[Mitochondrial Encephalopathy + Lactic Acidosis + Stroke-like episodes]

_________________

stroke-like episodes, lactic acidosis, seizures, m weakness, hearing loss
onset LOE40 yo
maternally transmitted only

Answer 84

A

[Non-Hodgkin Lymphoma: (DLBL)]

Diffuse Large B-Cell

_________________

RAS_{_HH_} O_{_RR_} PAI_{_NN_}

Answer 85

A

“Frostbite numbs_{your body}, scars_{your body}, _then Kills_{your body}”

1st: numbs ^{= [(Pallor +/- Thrombosis) + Anesthesia]}
2nd: scars^{= [blister + eschar]}
3rd: Kills ^{= [Deep Tissue Necrosis, Mummification]}

Answer 86

A

[Rapid rewarming in water bath at 37-39C] ;

Thrombolysis is considered in patients who:

have absent perfusion on angiography or technetium-99m scan
amputation would be suboptimal
seek care within 24h of injury (typically only used in these pts)

Answer 87

A

[FEVER + HA + THROMBOCYTOPENIA] in travelers returning from sub-Saharan Africa
Dx = peripheral blood smear
Plasmodium falciparum
[Antimalarial prophylaxis before, during and after]

Answer 88

A

BPH

“GSG cause Bleeds”

Answer 89

A

HyperCholesterolemia

“[herbs GSG] cause Bleeds”

Answer 90

A

Osteoarthritis

Answer 91

A

Osteoarthritis

Answer 92

A

Depression

_{Chronic alcoholics Steal Phen-Phen & Never Refuse Greasy Carbs which keeps them UP}

Answer 93

A

“[herbs GSG] cause Bleeds”
-Ginkgo biloba
-Saw Palmetto
-Garlic

Answer 94

A

Carbon & Nitrogen ; PLASTIC | Polyurethane foam

_{{{CYanide is released from [burning PLASTIC] or [Nitroprusside_Rx]} | Tx = Hydroxocobalamin_{+/- Sodium thiosulfate}}}

Answer 95

A

[CYanide^{(released from burning PLASTIC|using Nitroprusside_Rx)}] inhibits [mitochondrial oxidative phosphorylation] ➜ forces cell to switch to anaerobic metabolism ➜ lactic acid formation = [^{lactic acid}metabolic acidosis].

unused arterial oxygen remains in blood ➜ unused venous oxygen = [bright ^CHERRYRed skin]

_________________

tx = [Hydroxocobalamin +/- Sodium thiosulfate]

_{{CYanide tox sx = [bright ^CHERRYRed skin], Yucky bitter almond breath, brain⇪^*seizure*, brain⬇︎^{*CNS depression*} , [lung⇪ _f/b lung⬇︎]^{[tachypnea f/b bradypnea]}}

Answer 96

A

[CYanide (released from burning PLASTIC)] inhibits [mitochondrial oxidative phosphorylation] vs [CO binds hgb with higher affinity than O₂ ➜ DEC oxygen delivery]
[CO = Carboxyhemoglobin > 25%] vs [CYanide = nml Carboxyhemoglobin]

_________________

_{{{CYanide is released from [burning PLASTIC] or [Nitroprusside_Rx]} | Tx = Hydroxocobalamin_{+/- Sodium thiosulfate}}}

Answer 97

A

Bright CHERRY Red Skin (also seen in CO poisoning)
Yucky Bitter Almond breath
brain⇪^seizure
brain⬇︎^{CNS depression}
[lung⇪ _f/b lung⬇︎]^{[tachypnea ➜ bradypnea]}
[^lacticmetabolic acidosis]

🧠inhibits oxidative phosphorylation → anaerobic metabolism → lacticMA

_{{{CYanide is released from [burning PLASTIC] or [Nitroprusside_Rx]} | Tx = Hydroxocobalamin_{+/- Sodium thiosulfate}}}

Answer 98

A

CYanide;

▶Nitroprusside (rapid short acting vasoDilator) metabolizes into both:

Nitric Oxide ➜ vasoDilation
CYanide ➜ converted to thioCYanate ➜ RENAL excreted

_________________

▶Patients with renal insufficiency = unable to excrete thioCYanate ➜ CYanide toxicity

_{{{CYanide is released from [burning PLASTIC] or [Nitroprusside_Rx]} | Tx = Hydroxocobalamin_{+/- Sodium thiosulfate}}}

Answer 99

A

Factor 5 Leiden

Answer 100

A

blood is ordered for transfusion:

Type Serum Carefully, Dude

1st: Type: [Recipient patient’s] blood is typed = ABO and Rh determined

_________________

2nd: [Screen (PTAS)]: Recipient’s serum Screened for [unexpected preexisting autoantibodies (previously made against RBC antigens E, L or K from previous transfusions)] = [PreTransfusion Ab Screen]

_________________

3rd: Crossmatch Recipient’s blood with [blood they will be receiving] in-vitro first

_________________

4th: Decide: [_✅Transfuse(⊕unexpected _e/l/kRBC AutoAntibodies or ⊕Crossmatch rejection?)^{🚫Transfuse ➜ Identify Ab}]

Answer 101

A

Bone marrow; Organ ;

_________________

T ;

Skin
Liver
GI

This occurs because [Graft_Donor] T-cells recognize major and minor HLA antigens of the [Host_Recipient Skin//Liver/GI]

Answer 102

A

Leukoreduction of [graft_donor] blood

_________________

this will also ⬇︎ risk of HLA alloimmunization and CMV transmission

Answer 103

A

[Leukoreduction of [graft_donor] blood]
will ⬇︎ risk of:
1.[Febrile nonhemolytic transfusion reaction],
2.[HLA alloimmunization]✳
3.CMV transmission^{(CMV resides in Leukocytes)}

✳alloimmunization: ^{= *host_recipient immune response to otherwise [foreign antigens (blood group ag|histocompatibility ag) from ANOTHER PERSON] [⼀usually from incidental exposure like transfusion] *}

Answer 104

A

Cyanide toxicity

_{{{CYanide is released from [burning PLASTIC] or [Nitroprusside_Rx]} | Tx = Hydroxocobalamin_{+/- Sodium thiosulfate}}}

Answer 105

A

“superficial cut using DAG on it !”

1st: [aDherence] of circulating [inactivated platelet’s Gp1B] to exposed vWF of subendothelial collagen

→2nd: [aActivation & secretion] = Activated platelet → secretes fibrinogen and {[ThromboxaneA2 & ADP] → [INC (Gp2b/3a_platelet fibrinogen R) expression on platelets]}

→ 3rd: [aGgregation] of platelets via fibrinogen binding them together via [Gp2b/3a_platelet fibrinogen R]

= [weak 1º PLATELET PLUG]

______________________

Answer 106

A

platelet;

CKD patient
[1HS❌ (⇪ mucosal bleeding/bruising)]
[platelet count nl]
[PT/INR nl]
[aPTT nl]

__________________

1HS: [Primary Hemostasis platelet plugging]

Answer 107

A

a. platelet; [1HS❌ (⇪ mucosal bleeding/bruising)]

__________________

1HS: [Primary Hemostasis platelet plugging]

Answer 108

A

a. platelet; [1HS❌ (⇪ mucosal bleeding/bruising)]
* * *

c.

Sx = [desmopressin dDAVP (INC vWF secretion from endothelial cell)]^{IV or SQ}
Asx = observe

__________________

1HS: [Primary Hemostasis platelet plugging]

Answer 109

A

a. platelet;

[glanzmann thrombasthenia] ;

aGgregates platelets (—by binding [Activated platelet Gp2b/3A receptor] with a another [Activated platelet Gp2b/3A receptor] via fibrinogen)

b. “he ATE my Gp2b/3A”:

[Abciximab, Tirofiban, Eptifibatide]

__________________

Answer 110

A

a. platelet;

[Bernard-Soulier syndrome] ;

[aDheres [inactivated circulating platelets] to vWF ^{(which will already be bound to exposed subendothelial collagen)}

_{→platelet [Activation & secretion^{(of “F.A.T.” stuff)}] → platelet aGgregation = [DAG 1HS]}

Answer 111

A

ASA inhibits COX

✏️ { [platelet Arachidonic Acid] —(via COX)-→ converted to [TXA2 (thromboxane)] → [platelet TXA2 (ADP also)] INC expression of [Gp2b/3A_platelet fibrinogen R] which enables→ [platelet aGgregation] }

✏️ASA inhibits COX → No [TXA2 (thromboxane)]= No platelet aGgregation = No Clotting (“thins” your blood)

Answer 112

A

reversible or
time limited
(ex: surgery, pregnancy, OCP, trauma)
[Warfarin tx for only 3-6 months ( ≥6 mo for [1° idiopathic])]

Answer 113

A

depressed brain,* [= Somnolent/AMS]
depressed blacks,* [“-pupils” = miosis])
depressed breath* [= shallow bradypnea ≤12 RR]

Answer 114

A

[potent inhibitors of AChE]

→ [No ACh–breakdown] → [ACh accumulation] → hyperactivation of mCN receptors =

{[“OTC dUMBBELLS Create Muscle”] ? …….PAID}

[agricultural pesticides], [sarin_{(WARFARE AGENT)}]

_________________

mCN: muscarinic | CNS | Nicotinic

Answer 115

A

AChE ;

[ACh accumulation] → {[“OTC dUMBBELLS Create Muscle”] ? …….PAID}

[“OTC dUMBBELLS Create Muscle”]

Organophosphate _T_oxic Cholinergic :

[diarrhea/Urination/Miosis/Bradycardia/Bronchospasm_{( → Respiratory failure)}/Emesis/Liquid lung bronchorrhea /Lacrimation/Salivation]^muscarinic
[Coma/Seizure]^CNS
[Muscle(weakness/paralysis/fasciculation)]^Nicotinic

Answer 116

A

AChE ;

[ACh accumulation] → {[“OTC dUMBBELLS Create Muscle”] ? …….PAID}

PAID

[Pralidoxime ⼀reactivates AChE]
[Atropine anticholinergic⼀ competitively inhibits ACh]
[Intubation prn + ABCs (give activated charcoal if exposure ≤1h)]
[Decontamination]

Answer 117

A

DDDD^{(AKA Pellagra)}

Dementia

[Dry mouth^{STOMATITIS / CHEILOSIS}]

Diarrhea

[Dermatitis^{symmetrical/blister vesicles in sunexposed areas}]

💡Niacin uses Tryptophan for synthesis, & CaRcinoid tumors do also

Answer 118

A

areas of INC bone turnover;

osteoBLASTIC^{(prostate/SOLC/Hodgkin)}

Answer 119

A

Prostate / SOLC / Hodgkin

Answer 120

A

nMn*
N*onSOLC / Multiple Myeloma / NonHodgkin
- *

Answer 121

A

1.^{Dehydration =}[IV Hydration + IV Analgesia]
_________________
2.^{[Infxn (⊕fever|⊕WBC)] =}cefTriaxone
_________________
3.^Cold🌡=[Transfusion_{(if ⊕CVA|Retinal infarct|aCS| Priapism)}
_________________
4.^{“Kan’t breathe_hypoxia” =}[O2 + Hydoxyurea to carry more O2_⇪HbF]

treat the 4 SCD triggers (DICK)

aCS = acute Chest Syndrome

Answer 122

A

[Folic acid B9] chronically
Splenectomy (stops hemolysis)

Answer 123

A

NEVER!!!

give plasma EXCHANGE^{TTP tx}|supportive_{HUS tx}

_{TTP etx: [A13vM❌^{(or inhibition by shiga toxin in HUS)}] →uncontrolled vWF chain cleavage → widespread platelet traps/activation → thrombocytopenia + microagio hemolytic anemia → FMNRT TTP cp ^{⚠️TTP cp (aside from +Neuro and plasma EXCHANGE tx) = HUS cp}. ⼀ (TTP Tx = EXCHANGE plasma containing anti-A13vM or deficiency of A13vM for normal plasma)}

Answer 124

A

_1-6h[Febrile Nonhemolytic transfusion reaction] = F/C from cytokine accumulation during blood storage]

Answer 125

A

[DAT] and [fam hx]

AIHA = [⊕DAT] (negative fam hx)

_________________

Hereditary Spherocytosis = [⊝DAT] (positive fam hx)

DAT* = [Direct(Coombs) AntiHumanGlobulin Test]

Answer 126

A

IAT = [Indirect_Coombs AntiHumanglobulin Test] =

▶Uses [IAT and test blood] in lab to determine if h_r serum contain [preformed IsoAgglutinins^(IgM>IgG)] that agglutinate to common RBC antigens = “Antibody Screen”

▶Indirectly In Vitro: Mixes [test blood^{(which contain RBC loaded with common RBC antigens)}] with host_recipient’s [plasma w/antibodies]. ⼀ The IAT will bind to any {h_r [Ab|compliment (IgM/IgG/C3d/C3/etc.)} that have inappropriately agglutinated to RBC common antigens→ IAT is visualized to identify the RBC antigens (if any) h_r Ab are sensitized to.

[IAT = Indirect CAT]:
*CAT: Coombs AntiHumanglobulin Test] // [g_d: graft_donor] // [h_r: host_recipient]

Answer 127

A

DAT = [Direct_Coombs AntiHumanglobulin Test] =

[CAT: Coombs AntiHumanglobulin Test] // [gd\ : graft_donor] // [hr: host_recipient]

_________________

DAT

▶Uses CAT to determine if [^{gdRBC] are ACTIVELY being Sensitized (and ultimately hemolyzed) by [Transfusion/Drug-Induced/ ^hrIgM]}

▶DIRECTLY EN VIVO: host_recipient blood is taken and given CAT DIRECTLY → which will bind to (and allow us to visualize/identify) any {[hr\Ab|compliment ^{(IgM>>IgG/C3d/C3/etc)}] ACTIVELY agglutinating gd\RBC}

▶[⊕DAT is ALWAYS ABNORMAL] and usually comes from [host_recipient IgM and compliment] ^{(^{but incomplete DAT comes from IgG | compliment acting alone)}*}

Answer 128

A

DAT = [Direct_Coombs AntiHumanglobulin Test] =

[CAT: Coombs AntiHumanglobulin Test] // [gd\ : graft_donor] // [hr: host_recipient]

_________________

[⊕DAT occurs in ___]

[Acute Intravascular Transfusion Hemolysis]
[Delayed IgG EXtravascular Transfusion Hemolysis]
[Drug-Induced IgG EXtravascular Transfusion Hemolysis]
[Autoimmune Hemolysis]
[HDN (Hemolytic Disease of Newborn)]

Answer 129

A

_≤minutes[Anaphylaxis (IgA-deficient pts’ anti-IgA antibodies attack donor IgA)] = [Respiratory Distress, Angioedema]^{tx = Epi, antihistamine, CTS, [CardioPulm support]}
* * *
_{≤1 hr}[Acute Hemolytic Reaction (ABO mismatch 2/2 clerical error vs chronic transfusions) → [Preformed IgM using compliment (will have ⊕DAT)] → Intravascular hemolysis ] = ^[^T^achycardia/^L^umbarPain/^H^gbnuria/^B^{leeding_hypOtension_DIC/}^C^{hestConstriction/}^F^luLikeSx]^{tx = [NORMAL SALINE IVF]}

Answer 130

A

_≤minutes[Anaphylaxis (IgA-deficient pts’ anti-IgA antibodies attack donor IgA)] =

[Respiratory Distress, Angioedema]^{tx = Epi, antihistamine, CTS, [CardioPulm support]}

_{≤1 hr}*[Acute Hemolytic Reaction (ABO mismatch 2/2 clerical error vs chronic transfusions) → [Preformed IgM using compliment (will have ⊕DAT)] → Intravascular hemolysis ] =

[Tachycardia/LumbarPain/Hgbnuria/Bleeding_hypOtension_DIC/ChestConstriction/FluLikeSx]tx = [NORMAL SALINE IVF]

Answer 131

A

[monoclonal B-lymphocyte leukemia]; LATO sx

LAD

Anemia

Thrombocytopenia

Organomegaly^Liver/Spleen

[smudge cells_{(peripheral smear)}] and [flow cytometry]

Answer 132

A

Patients with

▨[limited CA: solely Organ/Organ’s lymph nodes] → limited bx^{organ or organ LN}]

▩ [EXTENSIVE CA: metastasis/involves supraclavicular LN → EXTENDED bx^{of one of the metastasized sites instead [(supraclavicular (if involved)] > other sites}]

= this is because metastasized sites (like Supraclavicular LN excisional bx) tend to be ⬇︎invasive and ⬇︎complications for biopsy

_________________

ex: Pts with suspected metastatic Lung cancer _{(if possible)}should have initial bx from one of the metastatic sites^{(SCLV-if involved) > other}

Answer 133

A

[NON-IgE] drug rxn involving vancomycin binding directly/activating mast cells → histamine release → [diffuse pruritus, erythema] ⼀proportional to infusion rate and resolved with d/c

Answer 134

A

s_x: “Monixide hurts my [MIND’S → SSSH]

Malaise

Irregularly SHARED HEADACHE (w/roommate, housemate, etc)

Nausea

Dizziness

Skin ∆^{[PINK-like cYanide tox] or [BLUE-like methemoglobinemia tox]}
* * *

Seizure/Syncope/Sleepy-COMA/Heart❌

tx: high-flow O2 via nonrebreather → hyperbaric oxygen

Answer 135

A

[high flow O2 via nonrebreather] –(if severe)–> hyperbaric oxygen

Answer 136

A

a. *^{(often confused for allergic rxn) *in seafood stored at temperatures > 15C, histidine undergoes decarboxylation → histaM**ine =
b. [flushing |throbbing HA|palpitations|abd cramps|diarrhea|(oral burning +/- “bitter taste”)] 10-30m after ingesting _(usually)FISH}

Answer 137

A

*perioral tingling

*paralysis

*poor coordination

Answer 138

A

[type 3 immune complex-mediated hypersensitivity rxn]
primarily occurs after receiving [antibodies_{Monoclonal/Chimeric}] or [antitoxins_heterologous]
SSLR = gzd urticaria + fever_{low grade} + arthralgia + LAD

_________________

SSLR: Serum Sickness-Like Reaction

Answer 139

A

{ allogenic hematopoietic stem cell transplant < [60 Y/O]< palliative care }

Answer 140

A

PANcytopenia ; [aPL ⼀acute PROMyelocytic Leukemia M3 (T15/17)]

Dx = smear showing [myeloblast>20%] –> flow cytometry for confirmation

Answer 141

A

[mild/moderate depression]

________________

It upregulates [CYP P450] ➜ ⇪ metabolism

_{Chronic alcoholics Steal Phen-Phen & Never Refuse Greasy Carbs which keeps them UP}

Answer 142

A

[somatostatin 14 analogue] ; [Somatotrope - Functional Pituitary Adenoma]

________________

inhibits [pituitary somatotrope] from releasing Growth Hormone in a [functional pituitary adenoma]

Answer 143

A

congenital bone marrow failure in infancy

________________

absent thumbs
craniofacial abnormalities
[SEVERE Macrocytic anemia (hgb < 9 at birth)]
reticulocytopenia

Answer 144

A

6 ^{= (this is the expected # lifetime Tetanus vaccines)}
_{#5 if 18 yo}

________________

[DTaP = (2 / 4 / 6 / 15 ) months old]

+

[TDaP at 11 years old]

+ TDaP _booster @ 21 years old

Answer 145

A

Steroids Make People Depressed!

Suicidality
Mania
Psychosis
Depression

Answer 146

A

“SSRI… {Sexually Slows & Really Impairs LEO”
⬇︎Libido | ⬇︎Orgasm | [⬇︎Ejaculation (delays)]

________________

[SWITCH to non-SSRI (buproprion/mirtazapine) ⚠️{DOSAGE reduce cautiously (for pts on high-dose/long term SSRI)}]

or

[AUGMENT with buproprion/sildenafil]

Answer 147

A

LCIS is nonmalignant, but still has ⇪ risk for development into [invasive breast CA or DCIS] = excisional biopsy + lifetime surveillance

Answer 148

A

d/c ALLforms of Heparin ➜ alternate anticoagulants (i.e. direct thrombin inhibitors) [even if no thrombosis present]

________________

platelet > 150K

Answer 149

A

[inhibits aldehyde dehydrogenase ➜ [SEVERE NV with any EtOH intake]
_________________

Disulfiram for [Die-Hard ABSTINENTS who want to stay Abstinent]

________________

Naltrexone ( ⬇︎EtOH cravings) for [moderate/SEVERE Alcoholism in opioid-free patients that are Alcoholic]

________________

[acamprosate (glutamate modulator)] is also used in Alcoholism

Answer 150

A

BRCA mutation > > > Klinefelter Syndrome

> [LAME (Liver failure/(Always Eating {Obese})/Marijuana/(Estrogen:androgen ratio ⇪ {gynecomastia})]

________________

BRCA = auto DOM mutations ➜ [⇪ Male Breast CA risk x 100]

[klinefelter syndrome XXY] = male having extra “X” chromo ➜ [Estrogen:androgen ratio ⇪] ➜ [⇪ Male Breast CA risk x 20]

Answer 151

A

60-100

(some can go down to 45 with no sx)

________________

Whipples = [low BG] + [PUSH low BG sx] + [PUSH low BG sx improve after glucose administration] = true hypOglycemia

________________

hypOglycemia sx = need PISH juice = Palpitations/Uneasy Irritable/Sweating/HA

Answer 152

A

AF ➜ RF

px = AF: [Allopurinol (xanthine oxidase inhibitor)] +Fluids IV]

________________

TX (for AKI 2/2 TLS) = RF: [Rasburicase (urate oxidase analogue)] + Fluids IV]

________________

[Allopurinol prevents Additional serum uric acid formation] whilst [Rasburicase metabolizes Realtime (already existing) serum uric acid]

Answer 153

A

Sickle Cell TRAIT = ASYMPTOMATIC (does not cause Anemia)

Answer 154

A

⭐caused by IL6 chronic inflammation → liver secretes hepcidin → [blocks ^{🆚 suspend}] {[DJ enterocyte ferroportin] and [macrophage ferroportin]} from transfering iron ^{from FerriTin_storage} to Transferrin_transport
⭐^{(→🔻TS_{(if ferroportin _blocked_)} 🆚 normal TS_{(if ferroportin only _suspended_)})},
⭐and exact opposite for FerriTin^{= 🔺_{*(ferroportin blocked) *} 🆚 nml_{(ferroportin suspended} FerriTin}

⭐but additionally❗️ all this hoopla also paradoxically keeps Transferrin out of circulation (^{which → ⬇︎TIBC (but with 🔻^/normalTransferrin Saturation)) = rare*}

⭐AND ULTIMATELY this ➜ {[(Normo^initially→micro^later)cytic] normochromic anemia}

*Typically Transferrin Saturation and TIBC are inverse related

so….
_________=________

^{iron studies =}{[_↧Transferrin Saturation _{with paradoxic}⬇︎TIBC]*,
[_↥FerriTin],
[⬇︎iron_{in circulation}^{iron in circulation is low because it’s still being sequestered to FerriTin by Hepcidin}]} =
{[_🢗MCV^{Normo –(to)–> micro} -CYTIC ] [NormoCHROMIC] }
___________________________x____________________________________
🔎DJ = Duodenal-Jejunal
🔎↧ = (DEC _or normal)
🔎↥ = (INC _or normal)
🔎TS = Transferrin Saturation

Answer 155

A

killing bacteria could ➜ ⇪ release of Shiga toxin

________________

SUPPORTIVE CARE ONLY

(fluid/electrolyte mgmt | blood transfusions | dialysis)

Answer 156

A

[ dopamine🟥 ] ; Huntington’s disease

Answer 157

A

SKIN

________________

Sweating = Stimulant tox

ALL Dry = Anticholinergic tox

Answer 158

A

⭐[B Cell CA (Multiple Myeloma)] ➜ Monoclonal immunoglobulins that aggregate at low temp < 37C = Cryoglobulins.

⭐Cryoglobulin precipitation ➜ noninflammatory microvascular occlusion and hyperviscosity sx when CG are high

_{hyperVIScosity sx = Vertigo, Imbalance/ataxia, Sight blurry}

Answer 159

A

FALSE

________________

Varenicline + NRT = ✔︎

Answer 160

A

_{osteoclast activating factor ➜}CUBP_sx

1.[(CRAB) - end organ damage]
_{hypercalcemia^{(→ vertebral dark lytic lesions/bone fx, constipation, depression)}}

Renal failure^{(2/2 Ig and Bence Jones proteinuria –> DEATH)}

Anemia normocytic

[Back pain i\ vertebral dark lytic lesions and bone fx]

________________

2.[Urine IgG or Urine IgA]

________________

3.[Bone marrow with ≥10% clonal plasmacytosis/plasmacytoma ^{(If Infection → DEATH!)}]

________________

4.[Protein (M Protein) in serum]

Answer 161

A

[Chronic Viremia/Autoimmune disease] ➜ [B cell hyperactivation] ➜ forms IgM which bind to IgG = ⇪ mixed circulating immune complexes

these [circulating immune complexes] desposit in small vessels ➜ INFLAMMATORY vasculitis (glomerulonephritis)

________________

Answer 162

A

Livedo reticularis
digital ischemia
retiform purpura (net like reflect of vasculature - image)

Answer 163

A

[1H-6H] ; [Fever / Chills / Malaise] _{(NO HEMOLYSIS)}
_________________
Leukoreduction =

⬇︎[Febrile nonhemolytic _{transfusion rxn}]

⬇︎HLA alloimmunization✳
[⬇︎CMV transmission ^{(since CMV resides in Leukocytes)}]

✳alloimmunization: ^{= *host_recipient immune response to otherwise [foreign antigens (blood group ag|histocompatibility ag) from ANOTHER PERSON] [⼀usually from incidental exposure like transfusion] *}

Answer 164

A

[HEMOLYSIS WITH UNCONJUGATED HYPERBILIRUBINEMIA → JAUNDICE]

[SUDDEN BACK PAIN]

FATIGUE

________________

X-linked RBC G6PD defect in African/Middle Eastern/Southeast asian ➜ ⇪ RBC hemolysis from [DASANI H₂O₂ oxidant stress]

Answer 165

A

✏️ [X-linked RBC (G6PD_Glutathione reductase) deficiency] in African/Middle E/SE asian

✏️= [“DASANI” H2O2 oxidant stress] → [RBC H₂O₂ ⇪ ^{(since there’s no G6PD to drive GSH buffer rxn which normally takes up oxidant stress)}] → [Oxidation denaturation of Hgb Sulfhydryl groups] = Formation of Heinz bodies in RBC→ [RBC damage and ⬇︎ membrane flexibility] = sx :

⬇︎

✏️a.. 🅸¹ = Intravascular hemolysis from [Oxidized denatured Hgb Sulfhydryl group membrane damage] → *[HEMOLYSIS WITH UNCONJUGATED HYPERBILIRUBINEMIA → JAUNDICE]**

✏️b.🅸²: [Heinz body RBC^{(RBC with oxidized denatured Hgb Sulfhydryl groups)}] travel thru splenic cord and splenic macrophages BITE out Heinz body] → [Bite RBC] –(eventually after enough bites) forms into→unstable Spherocyte} → 🅸

✏️c. 🄴Xtravascular hemolysis from [Heinz body-RBC] suddenly getting stuck in spleen → removed by splenic macrophages → [SUDDEN BACK PAIN] + FATIGUE

*🔎 🅸 = Intravascular hemolysis from membrane damage → [HEMOLYSIS WITH UNCONJUGATED HYPERBILIRUBINEMIA → JAUNDICE]**

Answer 166

A

[X-linked RBC (G6PD_Glutathione reductase) defect] in African/Middle E/SE asian

1.[measure G6PD activity]

2.[_{peripheral smear}:bite RBCs]

3.[_{peripheral smear}:[heinz body RBCs]^{(= accumulated “SHODE =byproducts of INC H2O2 on RBC)}]

SHODE: [Sulfhydryl Hgb ⼀ Oxidized, Denatured entities]

Answer 167

A

[Heinz body RBCs^{(accumulated oxidized denatured hgb sulfhydryl groups)}] in G6PD

GLUCOSE 6 PHOSPHATE DEFICIENCY

Answer 168

A

Spherocytes^{(Hereditary Spherocytosis | G6PD)}
_________________
Osmotic Fragility test

Answer 169

A

anemia that is
⼀microcytic (low mean corpuscular volume)
⼀hypOchromic (low mean corpuscular hgb)
[⇪ ferriTin (INC RBC turnover ➜ more iron to Tuck into storage)]
[normal RDW (all RBC uniformly made microcytic)]

_________________

Hgb electrophoresis: [βT minor = ⇪ HgbA2]

Answer 170

A

anti-platelet

________________

“I ATE [Gp2b/3A] for breakfast”

[ABCiximab / Tirofiban / EpTiFibatide]

Answer 171

A

hgb: M >18.5 | W>16.5

measure Erythropoietin
_________________
polycythemia? ➜ [**low EPO = polycythemia vera] vs [HIGH EPO = 2° polycythemia (chronic hypoxia or Renal Cell Carcinoma)]

Answer 172

A

hgb: M >18.5 | W>16.5
_________________

CHRONIC HYPOXIA

(consider carboxyhgb and sleep apnea)
_________________
polycythemia? ➜ [**low EPO = polycythemia vera] vs [HIGH EPO = 2° polycythemia (chronic hypoxia or Renal Cell Carcinoma)]

Answer 173

A

Doesn’t grow

Diaper rash

Dermatitis perioral

Diarrhea

Answer 174

A

AChE inhibitor –> TOO MUCH ACh in cleft –> [“OTC dUMBBELLS Create Muscle”] ? …….PAID

Organophospahtes are used in Agricultural Pesticides*
TX = Atropine + [Pralidoxime (reactivates AChE)]*

Answer 175

A

STATIN
_________________

[LDL ≥190]
[age ≥40 + DM]
[(10y ASCVD risk) ≥7.5%]

________________

THIS IS REGARDLESS OF BASELINE LDL

Answer 176

A

▶[X-linked recessive 1° immunodeficiency]

▶defect in [neutrophil (NADPH oxidase^{resp. burst})] ➜ impairs neutrophil superoxide formation ➜ [impaired neutrophil intracellular killing^{(neutrophils can eat BUT NOT KILL)}]

▶ = defective granuloma formation ➜ recurrent [catalase positive infections^{from “SPACE Bugs”}]

(Aspergillus = MAJOR COD / Staph A=liver/skin abscess/adenitis)

_{▶*(catalase+) infections = SPACE Bugs^{StaphA&Serratia/Pseudomonas/Aspergillus&Nocardia/Candida/Enterobacter/Burkholderia-cepacia</sup*
▶dx = nitroblue tetrazolium test}}

Answer 177

A

[(SMXTMP) + itraconazole]_px
_________________
[interferon-2]_tx

_{▶(catalase+) infections = SPACE Bugs^{StaphA&Serratia/Pseudomonas/Aspergillus&Nocardia/Candida/Enterobacter/Burkholderia-cepacia}
▶dx = nitroblue tetrazolium test}

Answer 178

A

▶*(catalase+) infections = SPACE Bugs^{StaphA&Serratia/Pseudomonas/Aspergillus&Nocardia/Candida/Enterobacter/Burkholderia-cepacia</sup*
_________________
[Chronic Granulomatous Disease]}

➜ (Aspergillus_ = MAJOR COD)

➜ (StaphA_=liver/skin abscess/adenitis)

_{dx = nitroblue tetrazolium test}

Answer 179

A

Metronidazole has Disulfiram-like activity –> _(toxic)Acetaldehyde accumulation –> Flushing/NV/Cramps after drinking

Answer 180

A

[Activated Charcoal (if within 4 h post ingestion)]

NAC is most effective when given within 8 hours post ingestion prior to hepatoxicity

Answer 181

A

during APAP OD,

APAP –(via CYP2E1)–> [toxic NAPQI] and [toxic NAPQI] depletes intrahepatic glutathione as it’s ➜ [NON-TOXIC cysteine & mercapturic acid]

once intrahepatic glutathione is all depleted [toxic NAPQI] accumulates ➜ hepatotoxicity

_________________

[Activated Charcoal (if within 4h post ingestion)]- binds APAP

[NAC (most effective within 8 hrs post ingestion)] ⇪ intrahepatic glutathione and restores [(toxic NAPQI) ➜ (nontoxic cysteine & mercapturic acid)]

_________________
protective < [EtOH chronicity] < exacerbant

Answer 182

A

during APAP OD,

APAP –(via CYP2E1)–> [toxic NAPQI] and [toxic NAPQI] depletes intrahepatic glutathione as it’s ➜ [NON-TOXIC cysteine & mercapturic acid]

once intrahepatic glutathione is all depleted [toxic NAPQI] accumulates ➜ hepatotoxicity

_________________

acute EtOH competes for CYP2E1 ➜ DEC [toxic NAPQI] = protective

CHRONIC EtOH upregulates CYP2E1 ➜ INC [toxic NAPQI] = exacerbant
_________________

[Activated Charcoal (if within 4h post ingestion)]- binds APAP

[NAC (most effective within 8 hrs post APAP ingestion)] ⇪ intrahepatic glutathione and restores [(toxic NAPQI) ➜ (nontoxic cysteine & mercapturic acid)]

Answer 183

A

suspected Alcoholic with:

AG met acidosis

INC osmolar gap

⊕ketones

variable blood glucose (DKA has BG > 250)
_________________
tx = [THIAMINE^1ST → Dextrose IVF^2nd]

dextrose will➜ insulin secretion ➜ metabolism of ketone bodies to HCO3

Answer 184

A

MentzeR Index = MCV/RBC

thalassemia < [MentzeR Index of 13] < IRON DEFICIENCY ANEMIA
_________________

Answer 185

A

Carcinoid tumors utilize Tryptophan to secrete tons of Serotonin. Tryptophan is also needed to make Niacin B3. This can –> Pellagra DDDD

Do not confuse Carcinoid Syndrome with VIPoma which presents similarly but VIPoma affects Pancreas while Carcinoid affects small intestine

Answer 186

A

BEN

Basophils

Eosinophils

Neutrophils

Clozapine also causes Metabolic Syndrome X, Seizures and Myocarditis

Answer 187

A

actinic solar keratosis

anogenital warts

superficial Basal Cell Carcinoma

Answer 188

A

Buspirone = [5HT1α R partial agonist]

________________

GAD

________________

[slow onset] and [lacks muscle relaxant/anticonvulsant properties]

Answer 189

A

s_x: “Monixide hurts my [MIND’S → SSSH]

Malaise

Irregularly SHARED HEADACHE (w/roommate, housemate, etc)

Nausea

Dizziness

Skin ∆^{[PINK-like cYanide tox] or [BLUE-like methemoglobinemia tox]}
* * *

Seizure/Syncope/Sleepy-COMA/Heart❌

________________

Dx = [ABG Carboxyhemoglobin levels]

⚠️ _{Monoxide tox can present very similarly to [cYanide tox (which is also [PINK SKIN BUT with Yucky bitter almond breath)] and [Methemoglobinemia tox (BLUE SKIN)] so be careful!}

Answer 190

A

{carbon Monoxide tox^{(MIND’S → SSSH)} ➜ [PINK SKIN]}

________________

{CYanide tox ➜ [PINK SKIN with Yucky BITTER ALMOND BREATH]}

Answer 191

A

1978

false positives occur so be sure to confirm with venous blood draw!

Answer 192

A

“cYaMonoxide toxicity Needs Overt Smoke Help”

empiric tx for cYanide and ^(carbon)Monoxide toxicity

[Nitrites^{(induces methemoglobinemia)}]
Oxygen 100% (CO tx)
[Sodium thiosulfate]
[HydroxoCoBalamin^{(binds cYanide ➜ excretable cYanocobalamin)}]

________________

empircally treat smoke inhalation pts for CYanide tox!

Answer 193

A

[SEVERE <28C (or unresponsive Moderate)]:

[ACTIVE CORE REWARMING (WARM PERITONEAL LAVAGE, WARM HUMIDIFIED O2)]
_________________
{“(C_ut ) BLM!”_{–tx–> [ACTIVE CORE🔥]}}

BLM = Brain/Liver&heart/Muscle

{“(Cut) BLM”_{–tx–> [ACTIVE CORE🔥]}} =
🧠 Brain^{= _C_OMA}
🫁Lungs/heart^{= _C_ardiac Vt arrhythmia}
💪Muscle^{= _C_V Collapse}

Answer 194

A

[Moderate 28-32C (or unresponsive mild) hypOthermia]:

[ACTIVE e🅇ternal warming *(heated blankets, heated baths, heated forced air) *]
\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_

{*"(slow) BLM"*--tx--> [ACTIVE🅇🔥]}

| BLM = Brain, [Lungs&heart, Muscle] || 🅇=E🅇ternal

## Footnote

{*"(slow) BLM"*--tx--> [ACTIVE🅇🔥]} =
🧠 *Brain*lethargy
[🫁&🩷]*Lungs&heart*hypOventilation, bradycardia/_atrial_ arrhythmia, 
💪*Muscle*DEC shivering

Answer 195

A

[mild 32-35C hypOthermia]:

[passive external warming ^{( warm blankets & remove wet clothes)}]
_________________
{“(FAST) BLM”_{–tx–> [passive^🅇🔥]}}

BLM = Brain, [Lungs&heart, Muscle] || 🅇=E🅇ternal

{“(FAST) BLM”_{–tx–> [passive^🅇🔥]}} =
🧠 Brain^{ataxia, dysarthria}
🫁Lungs/heart^{tachypnea/tachycardia}
💪Muscle^{INC shivering}

Answer 196

A

b. Streptokinase , Urokinase
c. Aminocaproic acid

Answer 197

A

[^{(mild ⬇︎ only)}anxiety^{][(mild ⬇︎ only)}insomnia ]
_________________
[LIVER FAILURE weeks after starting it]

Answer 198

A

[NaHCO3 IV] ➜ [HemoDialysis (if severe)]
_________________

[NaHCO3 IV] Alkalinizes Blood and Urine ➜ basic blood/urine environment ➜ deprotonation of Salicylates ➜[Salicylate ion] inability to be reabsorbed into CNS or into [blood from renal tubules] ➜ [⇪ salicylate ion excretion]

severe = cerebral/pulmonary edema | renal failure

Answer 199

A

venous lead level
_________________

lead tox ➜ neurobehavioral impairment. tx = AVOID LEAD EXPOSURE

Answer 200

A

[isolated stomach fundal varices] -> variceal hematemesis
[splenomegaly] -> anemia/thrombocytopenia

Splenic Vein Thrombosis is commonly a/w pancreatitis

Answer 201

A

Can cause SIGNIFICANT K+ RELEASE –> VFIB in pts at high risk for Hyperkalemia

Answer 202

A

Aerobic = 32

AnAerobic = [2 + Lactate]

Answer 203

A

abnml proliferation of plasma cells that produce useless immunoglobulin (IgG , IgA) –> [Osteoclast Activating Factor] which → CUBP

When MM produces IgM = WaldenstroM Macroglobulinemia

CUBP
1.{[CRAB end organ ❌]_{(hyperCalcemia), Renal Failure 2/2 bence jones proteinuria, Anemia_normocytic, Back pain i\lytic bone fx}}
_________________
2.[Urine IgG/IgA]^{get urine immunoelectrophoresis}
_________________
3.⚠️ [Bone marrow >10% plasmacytosis]^{CONFIRMS MM DX}
_________________
4.[Protein^{(serum: M protein, IgG, IgA [monoclonal “M” spike if MGUS & smear: Rouleaux )}]

Answer 204

A

CUBP
1.{[CRAB end organ ❌]_{(hyperCalcemia), Renal Failure 2/2 bence jones proteinuria, Anemia_normocytic, Back pain i\lytic bone fx}}
_________________
2.[Urine IgG/IgA]^{get urine immunoelectrophoresis}
_________________
3.⚠️ [Bone marrow >10% plasmacytosis]^{CONFIRMS MM DX}
_________________
4.[Protein^{(serum: M protein, IgG, IgA [monoclonal “M” spike if MGUS & smear: Rouleaux )}]

Answer 205

A

Prostate
Renal
Lung
Breast
Multiple Myeloma

Answer 206

A

[Thiamine B1]

Answer 207

A

ATP;

Think ATP: [Thiamine B1] is needed to catabolize glucose into ATP with the “αTP” enzymes :
[α-ketoglutarate dehydrogenase (TCA)],
[Transketolase (HMP shunt)],
[Pyruvate dehydrogenase (TCA)]
_________________

_{💡so… if [Thiamine B1] deficient ➜ “αTP” enzyme [impaired glucose metabolism → ATP depletion] which → [Wernicke Korsakoff Syndrome] and [BeriBeri]}

_{📖[BeriBeri falls into 3 subtypes ^{(WET, DRY, BOTH)}] :}

1.[High Output Dilated HF + edema] = WET

2.[Symmetrical Peripheral Neuropathy + muscle wasting] = DRY

3.[WET and DRY]^(BOTH)

Answer 208

A

a. >100
_________________

b.
1st: _ASA-induced[AG metabolic acidosis] ➜
2nd:_compensatory[respiratory alkalosis] =
3rd: [MIXED AG metabolic acidosis WITH respiratory alkalosis]

“Air HOT/[Sound ringing-stomach sick]/Air fast”

Answer 209

A

Acute Aspirin ingestion ➜ vomiting

“acute A S A gets you Sick to ur Stomach^(vomiting)!”

Answer 210

A

ASA –> [Mixed Respiratory alkalosis + AG metabolic acidosis] (Normal pH/DEC PCO2/DEC HCO3)

[Air is Fast (Tachypnea)]
{[Sound ringing (Tinnitus)] … _and [Stomach Sick (Vomiting)]}
[Air is Hot (Fever]

Answer 211

A

ASA;

COX inhibitor –> DEC [Thromboxane A2] –> DEC Platelet aggregation and vasoconstriction

_{✏️Activated platelet → secretes fibrinogen and {[ThromboxaneA2 & ADP] → [INC (Gp2b/3a_platelet fibrinogen R) expression on platelets]}}

Answer 212

A

⏸️[COMPENSATED arterial PaCO2^{(compensating for acute metabolic∆|acute renal∆)}]

⏸️should be within
⏯️ {^{+/- 2 of}[1.5 x HCO3 + 8]} …

⏏️…If not = [mixed acid/base picture]

Answer 213

A

“treating unknown OD ingestion is a BITCH”
1. Bicarb IV ^{(NaHCO3 IV → ⇪ ASA excretion)✏️}
2. [iPecac syrup (if alert)]^{= induces emesis}
3. Toss out Gastric contents with [Gastric lavage (if within 1 hr of ingestion)]
4. [Charcoal activated]^{= absorbs ingested toxin}
5. Hemodialysis

^{📝<(NaHCO3 IV alkalinizes urine and blood → deprotonates salicylate → salicylate ion can’t cross membrane = no renal reabsorption or BBB crossing}

Answer 214

A

[initial salicylate > 160] mg/dL
[6 hr salicylate > 130]
persistent acidosis pH < 7.1

Answer 215

A

Anticholinergism!
1.mad\hatter{delirium, seizure}, 2.blind\bat,
3.dry\bone{dry mouth}
4.hot\hare{HYPERthermia}
5.bowel-bladder lose [contraction] tone{urinary retention}
6. heart runs LONG{[6a. Widened QRS > 100ms ➜ Arrhythmia]_NaHCO3^IVtx] & 6b.Prolonged intervals}

Answer 216

A

[NaHCO3]^IV = for QRS widening or Ventricular arrhythmia
Activated charcoal if within 2h ingestion
Intubation/oxygenation
IVF

Answer 217

A

In Cardiac tissue, Sodium Bicarb [⬆︎extracellular sodium] and [⬆︎ extracellular pH] to alleviate TCA’s cardio-depressant action on sodium channels

Answer 218

A

QRS duration

___________

QRS > 100ms –> INC Vt arrhythmias and seizures (tx: NaHO3^IV)

Answer 219

A

_{DVT #1 = {[rafX Factor 10a inhibitor] x ≥3mo}_tx}

Answer 220

A

FALSE!!!!!!!!

PATIENTS WITH HITT ARE HEPARIN-BANNED FOR LIFE!!

Answer 221

A

DAB
1. Dabigatran
2. Argatroban
3. Bivalirudin

-bivalirudin is related to hirudin (anticoagulant leeches use)
-Use [Direct Thrombin Factor 2a inhibitors] in patients with HIT

Answer 222

A

DISCONTINUE ANY HEPARIN
start _DAB[Direct Thrombin Factor 2a inhibitors] or
start [fondaparinuX_{(factor 10a inhibitor)}]

Answer 223

A

HITT2 = all 4T score

Thrombocyte DEC GOE30-50%
Timing onset 5-10d after Heparin exposure (or 1d if previous exposure)
Thrombosis present
Took Out other thrombocytopenia causes

Answer 224

A

[HITT1] = NONIMMUNE Heparin-Platelet clumping] ➜ [platelet > 100K] and resolves spontaneously

Answer 225

A

WHITE EYE REFLEX;

Retinoblastoma

Answer 226

A

DECREASED

________________

Liberated Hgb (after RBC hemolysis) BINDS to serum Haptoglobin –> HgbHaptoglobin complex –> Cleared by Liver

Haptoglobin picks up Haphazard hgb

Answer 227

A

FALSE!

NonSOLC _{brain metz} = NONchemoSensitive

Answer 228

A

A-I-P causes N-A-P

Psychosis acute onset
Abd pain acute onset
Neuropathy acute onset

Fam hx of this is VERY suggestive of AIP

Answer 229

A

________________

enzyme❌is associated with [| ⬜]

Answer 230

A

Sideroblastic anemia

Answer 231

A

Thalassemia (except 3 gene deletion alpha thalassemia)

Dx = Hgb electrophoresis with genetic studies if alpha thalassemia

Answer 232

A

Pyridoxine B6

Answer 233

A

PERNICIOUS ANEMIA = MOST COMMON CAUSE
Vegan/Vegetarian
Blind loop syndrome (Gastrectomy or RYGB)
Diphyllobothrium latum
Pancreatic Insufficiency
Terminal iLeum damage (Crohns)

Answer 234

A

Vitamin B12 isomerizes methymalonyl coA in the spinal cord myelin —> succinyl coA.

Without it –> suBACute combined degeneration

usually manifest as paresthesia/peripheral neuropathy

Answer 235

A

Pigmented bilirubin gallstones

Answer 236

A

Howell Jolly Bodies = [^RBCbasophilic nuclear remnants(usually removed by spleen macrophages)] = Pts with autosplenectomy/asplenia^{(i.e. from Sickle Cell Disease)} = will not be able to remove [Howell Jolly Bodies]

Answer 237

A

Ehrlichia infection

Answer 238

A

Hep C
Joint Pain
Glomerulonephritis

Answer 239

A

TTP etx: [A13vM❌^{(or A13vM inhibition by shiga toxin in HUS)}] →uncontrolled vWF chain cleavage → widespread platelet traps/activation → severe thrombocytopenia + [RBC shearing ⼀ microangiopathic hemolytic anemia]) → FMNRT TTP sx ^{⚠️TTP cp (aside from +Neuro and plasma EXCHANGE tx) = HUS cp}.

(TTP Tx = EXCHANGE plasma containing anti-A13vM or deficiency of A13vM for normal plasma)

Answer 240

A

CLOpidogrel
tiCLOpidine
cyCLOsporine
AIDS ^{“CLOset gay”}
{Pregnancy^{TTP can onset anytime during [gestation or postpartum pregnancy]}} ^{“CLOset Mom”}

Unlike HUS, [TTP = (neuro sx^{(confusion/seizure)}) / fever / (plasma EXCHANGE _tx)]

_{TTP etx: [A13vM❌^{(or inhibition by shiga toxin in HUS)}] →uncontrolled vWF chain cleavage → widespread platelet traps/activation → thrombocytopenia + microagio hemolytic anemia → FMNRT TTP cp ^{⚠️TTP cp (aside from +Neuro and plasma EXCHANGE tx) = HUS cp}. ⼀ (TTP Tx = EXCHANGE plasma containing anti-A13vM or deficiency of A13vM for normal plasma)}

Answer 241

A

Prednisone
Bone Marrow Transplant = cure
Eculizumab (inactivates C5 complement)

Answer 242

A

Polycythemia Vera

________________

JAK2 mutation (r/o hypoxia)

________________

Remember: PV ⬆︎ALL 3 cell lines but places focus on RBC more
You must exlude Hypoxia as a cause of ⬆︎RBC

Answer 243

A

phlebotomy
hydroxyurea^{Inhibits [Ribonucleotide Reductase] –> inhibits [DNA thymine] synthesis→ ⬇︎cell synthesis}
. [ASA ^{for erythromelalgia (painful red hands from ET or PCV)}]

Answer 244

A

ONLY when

pt>60 yo with sx

OR

pt>60 with [platelets>1.5million]

Answer 245

A

HYDROXYUREA^{Inhibits [Ribonucleotide Reductase] –> inhibits [DNA thymine] synthesis}
[Anagrelide ^{when RBC is suppressed from Hydroxyurea}]
[ASA ^{for erythromelalgia (painful red hands from ET or PCV)}]

Answer 246

A

ALL
AML
[aPL_{- acute Promyelocytic Leukemia M3 (chromo T15/17)}]
Aplastic Anemia^{(Radiation|drugs|Viruses|Fanconi|Idiopathic)}
[CIPM - Myelofibrosis (dry tap and tear drop cells)]
[Myelodysplastic Syndrome (hypercellular bone marrow with ringed sideroblast RBC with Prussian blue )]
[Hairy Cell Leukemia (dry tap with hypercell bone marrow)]

Answer 247

A

PANcytopenia

________________

[aPL - acute Promyelocytic Leukemia M3 (chromo t1517)]

Dx = smear showing blast –> flow cytometry for confirmation

Answer 248

A

❗️[CML^{(9/22 BCRABL)}] ⇪ Granulocyte proliferation ⼀

❗️[infection (Leukamoid Stress Reaction)] also ⇪ Granulocyte proliferation ⼀

❗️but [CML Leukemia CA cells] do NOT have high levels of [Leukocyte Alkaline Phosphatase] and

❗️ ❗️ so… ⇪Granulocytes? Check LAP

⭐[_CML(LAP elevated?)^INFECTION]

_________________

CML: Chronic Myelogenous Leukemia

Answer 249

A

tx = [tyrosine kinase inhibitors ( x-tinib)] such as ..

imatinib
dasatinib
nilotinib

Cure = Bone marrow transplant (NEVER the first therapy though)

Answer 250

A

✏️[neutrophils with 2-lobe nuclei^{(instead of the normal 3-lobe nuclei)}]

2/2 [de novo mutations vs exposure^{(radiation, benzene, chemotherapy)}] → dysfunctional hematopoiesis (defective cell maturation) of Myeloid cells^{(risk of transformation to AML :-( )}

✏️MyeloDysplastic Syndrome

Answer 251

A

proliferation of normal and mature (but dysfunctional) B lymphocytes with smudge cells

Answer 252

A

conversion of CLL–> [high grade lymphoma^{(DLBL or Prolymphocytic Lymphoma)}] which happens in 5% of patients

________________

CLL = mature lymphocytes and smudge cells

Answer 253

A

[2CDA_Cladribine_{adenosine analog}]

Answer 254

A

NHL = solid mass (lymph nodes and spleen)

CLL = Circulating liquid mass (so use flow cytometry of peripheral blood to diagnose)

Answer 255

A

nHL Dx = [Xbx with CTS ➜ Bbx ^{for tx}]

_________________
[EXCISIONAL bx with CT staging]

_and

[B_oneM_arrowbx to determine tx]

________________

nHL dx = HODGKIN LYMPHOMA dx- (except HL also requires [⊕ReedSternberg CD15 & CD30 owl eye cells]) =

HL Dx = i\⊕CD15 and ⊕CD30[Xbx with CTS ➜ Bbx ^{for tx}]

Answer 256

A

CHOPX

Answer 257

A

1 = R_{adiation_local}
2 = R_{adiation_local}
3 = CHOPX
4 = CHOPX

Answer 258

A

1 = R_{adiation_local}
2 = R_{adiation_local}
3 = BHOD
4 = BHOD

Answer 259

A

STAGING^{= MOST IMPORTANT PGN} > [(Lymphocyte RICH) ^{= GOOD Pgn}]

[(Lymphocyte mixed) and (Lymphocyte poor))]^{= poor pgn}

Answer 260

A

Determine cardiotoxicity for Adriamycin/Doxorubicin tx used for Hodgkin Lymphoma

Answer 261

A

“his DIC SCABS Terribly!”

Sepsis
CA
Abruptio placenta or Amniotic fluid embolus
Burns
Snake bites
Trauma –> tissue factor release

DIC activates primary AND secondary coagulation

Answer 262

A

[FFP^{(contains clotting factors but req 2L dose)}]
[Cryoprecipitate^{(contains clotting factors, vWF, and replaces fibrinogen if FFP doesn’t work)}]
Platelets if < 50K

“his DIC SCABS Terribly!”

Answer 263

A

Venous

________________

[Platelet factor 4 Ab on ELISA] or [Serotonin release assay]

Answer 264

A

PCN PO QD

x 5 years

Answer 265

A

Superficial Bleeding out of proportion to the degree of thrombocytopenia
GIANT platelets

etx = absent [platelet glycoprotein 1B R] for von willebrand factor to bind to

Answer 266

A

stabilizes bony metastatic lesions which

prevents _CAhypercalcemia
prevents _CA fx

Answer 267

A

Megestrol^{progesterone analogue}

> >>> CTS

Marijuana is only useful in HIV anorexia

Answer 268

A

Hgb<10 (use EPO with hct goal of 35%)

________________

HTN
HA
Flu-like sx

Answer 269

A

[Fanconi ^P-A-N anemia] = DNA repair defect

that → [CPMSC❌ ^{(failure/destruction/suppression)}) = Aplastic Anemia] →

[^{Aplastic Anemia}PANcytopenia marrow failure] → [mucosal bleeding/petechiae], [NORMOcytic but hypOproliferative anemia], infection
morphological changes
growth stunt

🔎CPMSC = [Common Progenitor Myeloid Stem Cell]
🔎P-A-N = [Pancytopenic-Aplastic-Normocytic]

Answer 270

A

⬆︎ABSOLUTE BASOPHILIA
⬆︎⬆︎⬆︎LEUKOCYTOSIS
shift tward precursor cells (myelocytes or promyelocytes)
⬇︎Leukocyte Alkaline Phosphatase (LAP)

Cure = Bone marrow transplant (NEVER the first therapy though)

etx = 922 BCRABL philadelphia chromosome

Answer 271

A

“CML has L-L-L-“
[Leukocytosis _with LOW LAP]

❗️ LAP = Leukocyte Alkaline Phosphatase = marker of [natural *leukomoid *neutrophil activity]. leukomoid rxn → ^HIGHLAP

Answer 272

A

AUTO DOM point mutation in Factor 5 gene –> RESISTANCE TO PROTEIN C (which is supposed to inactivate Factor 5). This –> Hypercoagulability

aPTT AND PT/INR may both be normal!

Answer 273

A

E5 with Acid

[Eosin 5 maleimide binding flow cytometry] WITH [Acidified glycerol lysis test]

OR

Osmotic fragility test but it has low sensitvity

Lab findings = ⬆︎Mean Corpuscular Hgb Concentration

Answer 274

A

_{[🩸 = “RBC membrane”]*}
🟠[🩸Spectrin’s inability to anchor [AUTO DOM defective 🩸Ankyrin] → [🩸 bleb formation] –> splenic macrophages remove but hemolyze/damage RBC in process➜ [JAUNDICE unconjugated hyperbilirubinemia],
_________________
🟠 over time, splenic macrophages hypertrophy → [SPLENOMEGALY]. And [RBC∆^{(⬇︎MCV with ⇪MCHC, biconcave → spherical)} → [High RDW] = [“SPHEROCYTE” RBCs]
_________________
🟠 ULTIMATELY, [SPHEROCYTE RBC ∆ ^{(small, spherical, no central pallor)}] → [splenic macrophage premature removal altogether → [*eXtravascular hemolytic anemia ] ^{Tx = Splenectomy}

🔎MCHC = Mean Cell Hgb Concentration

Triad = Jaundice, Splenomegaly, Hemolytic Anemia

Answer 275

A

{[Hereditary Spherocytosis_{Chronic Hemolysis}]

Triad = Jaundice, Splenomegaly, Hemolytic Anemia

_{HS –(pigmented bilirubin gallstones)–>[Acute Cholecystitiss]}}

Answer 276

A

because ONLY in the petri dish, it causes prolonged aPTT

Answer 277

A

hypercoagulable disorder –> recurrent migratory superficical thrombophlebitis at unusual sites (arm, chest)

________________

Pancreatic Cancer (or sometimes stomach, lung or prostate)

Answer 278

A

GENETIC! Whites of Northern European ancestry naturally develop Pernicious Anemia

also, Pernicious Anemia ⬆︎ risk for gastric ADC

Answer 279

A

▶Warfarin inhibits epoxide reductase (which reduces⼀activates Vitamin K^{(K is responsible for maturing [2, 7, 9, 10, Protein C and S])}→ ⬇︎[2,7,9,10, Protein C and S]

▶2,7,9,10 = ⬆︎Clotting

▶[Protein C and S] = anti-Clot = Bleeding.

⭐But since Protein C and S are the first to be affected by warfarin, allowing 2,7,9,10 to roam freely and ⬆︎Clotting

Answer 280

A

Gastric ADC

Answer 281

A

Diamond Blackfan Syndrome (DBS)

intrinsic defect in erythroid progenitor cells –> ⬆︎apoptosis

Answer 282

A

Atypical Reactive CD8 T cells; Infectious Mononucleosis

Answer 283

A

B cell neoplasm that infiltrates bone marrow, spleen and peripheral blood; Bone Marrow Biopsy

Answer 284

A

Gaucher ; lysosomal storage disease

Answer 285

A

“T ransferrin _I_n _B_lood _C_alculation”
-TIBC gives a snapshot ^{(for that that moment in time)} of how much iron the body:
-can carry ^{(TIBC indicates total capacity [for that moment] the body has to transport iron). ⇪ capacity/TIBC may indicate ⇪ demand)}
-wants to carry (demand)

Answer 286

A

⬇︎MCV

⬆︎Iron

Answer 287

A

1._{peripheral blood FLOW CYTOMETRY}proliferation of [normal, mature (but dysfunctional) B lymphocytes]

with

2._{peripheral blood smear}smudge cells
* * *

_{Suspect CLLSLL in any elderly with dramatic leukocytosis primarily made of lymphocytes}

Answer 288

A

Phlebotomy (tx for PV) removes cells while Plasma exchange only removes substances (Antibodies, immune complexes, toxins)

Answer 289

A

Leydig ; Testosterone AND Estrogen

All Solid Testicular Tumor Masses should be treated with Radical Orchiectomy

Answer 290

A

“Discern {[EBR^{[Echinocyte/Burr=Renal🌀]} _from ASL^{[Acanthocyte/Spur(ky)=Liver🌀]}] _{⼀red blood cells}}!”
_________________

[Acanthocyte Spur_ky RBC] = [L_{iver🌀 | Cholesterol❌}]

[Acanthocyte Spur RBC] are Spurky = Spiky!

🌀 = disease

Answer 291

A

Hereditary Spherocytosis

Answer 292

A

Osler Weber Rendu likes to EAT

Epistaxis recurrently
AV malformations
Telangiectasia

Answer 293

A

[Pyridoxine B6] with [Folate B9]

Answer 294

A

[ferrous sulfate 2+ _ heme iron]

”give *us 2 more iron”*

Answer 295

A

Polycythemia Vera

________________

Heat ⬆︎Basophils (rare but can become AML) –> ⬆︎Histamine release

________________

Remember: PV ⬆︎ALL 3 cell lines but places focus on RBC more

Answer 296

A

[TRAP-Tartrate Resistant Acid Phosphatase]

or

CD11c

Answer 297

A

painLESS LAD
B sx (Fever, Night sweats, Wt Loss)

Dx = EXCISIONAL bx with staging via CT and BMbx to determine tx

THIS IS THE SAME AS HODGKIN LYMPHOMA - except HD has ReedSternberg owl cells

Answer 298

A

[(⬆︎Porphobilinogen) in Urine]

________________

Fam hx of similar sx

Answer 299

A

(UROPorphyrinogen)

⬇︎

<UROPorphoDeCarb | PCT> “UPDC PCT”

__________________

AAPUF
enzyme is associated with [| x]

Answer 300

A

{[CoproPorphyrinogen^{in cytoplasm} (enters mitochondria)→ Protoporphyrin^{in mitochondria}] + Fe²⁺ }

⬇︎

⬇︎

⭐HEME⭐

__________________

AAPUF
enzyme is associated with [| x]

Answer 301

A

(ALA)

⬇︎

__________________

AAPUF
enzyme is associated with [| x]

Answer 302

A

(Porphobilinogen)

⬇︎

__________________

AAPUF
enzyme is associated with [| x]

Answer 303

A

[(Glycine) + (Succinyl CoA) + (Pyridoxine B6)]

⬇︎

__________________

AAPUF

enzyme is associated with [| x]

Answer 304

A

cp = HOT

[Head ❌(CNS dysfxn/confusion/weakness/seizures)]

[Organ ❌(ARDS/Pulm Edema/NV/Liver Injury/AKI/Rhabdomyolysis/DIC)]

[Temp core > 40C (104F)]

Answer 305

A

cp = HOT

tx = evaporative /convective cooling with water misters and fan

Answer 306

A

herbal teas;

Answer 307

A

⬇︎O2 carrying capacity in blood

C^LDP

LDP

[Loss of RBC Blood Volume]^{(Melena, Hematochezia, Ulcers, Fibroids)}

[Destruction of RBC (Hemolytic Anemia)]^{Intrinsic|Extrinsic in Intravascular|Extravascular}

[Poor production of RBC (⬇︎Erythropoiesis)]

Answer 308

A

⬇︎O2 carrying capacity in blood

* * *
*i*\_**TAILS**

\_\_\_\_\_\_\_\_\_\_\_

m*_i_*crocytic

Answer 309

A

⬇︎O2 carrying capacity in blood

* * *
*am*\_**FOB**
*an*\_**LAR**

\_\_\_\_\_\_\_\_\_\_\_

m*_a_*crocytic

Answer 310

A

⬇︎O2 carrying capacity in blood

* * *

m*_a_*crocytic ;

1. MOD: [auto recessive **defective UMP synthase**] → inability to convert orotic acid to UMP during pyrimidine synthesis. =
2. [macrocytic Megaloblastic anemia (*am\_FOB*)] in kids that ultimately → Failure to Thrive
3. can NOT be cured with *F*olate or *B*12
4. NO hyperammonemia(ornithine transcarbamylase deficiency = ⇪ orotic aciduria WITH hyperammonemia)

Answer 311

A

⬇︎O2 carrying capacity in blood

* * *

[*Nn***\_CATIA**]

[*Nhi*\_**GHSPCP**]

[*Nhe*\_**MAIM**]

Answer 312

A

varying sizes of RBC

Answer 313

A

varying shaPes of RBC

Answer 314

A

[Thrombocyte platelet]

_________________

[endothelial tissue injury in 1º hemostasis] ;

[Thrombocyte platelet] plug after aggregating with other [Thrombocyte platelets] and interacting with fibrinogen

⅓ platelets are stored in spleen

Answer 315

A

Neutrophils Like Making Everything Better

Neutrophils

Lymphocytes

Monocyte_macrophages

Eosinophils

Basophils

Answer 316

A

start with cell age

Acute
1. [Acute>Lymphoid]= ALL
2. [Acute >Myeloid]= AML
* * *
Chronic

[Chronic>Lymphoid>Chronic Leukemia= C|H|A]
[Chronic>Lymphoid>Lymphoma={Hodgkin vs [NonHodgkin^”^{🆃all 🅱}^{rian Forgot Mr Burkitt’s Dogg”}^|]}
[Chronic>Lymphoid>Plasma cell disorders=MultipleMyeloma | Waldenstrommacrogloulinemia, MGUS]

_________________

[Chronic>Myeloid>Myeloproliferative disorders* (Constitutively Activated Tyrosine Kinase → Myeloproliferative disorder) = 1|P|E|C]^([^1º^{Myelofibrosis/CIM] | [}^P^{olycythemia Vera] | [}^E^{ssential Thrombocytosis] | [}^C^{hronic Myelogenous Leukemia]}

Answer 317

A

immature neutrophils;

{ [⇪ mYeloblast (precursor to BEN_granulocytes)] proliferation^{( = bacterial infections or CML)}]}

Answer 318

A

“NAACP for E-Osar-N-Phil”

Neoplasia

Asthma^{(limits rxn after mast cell degranulation + produces Histamine)}

Allergy

Connective tissue disease

Parasites_invasive^{(targets Major Basic Protein = protects from Helminth)}

Answer 319

A

basophil ; Tryptase

Histamine & Heparin are also released

Answer 320

A

[8^cMyc ➜ 14^{IG-Heavy Chain}]; [cMYC^{(and EBV INC B- cell proliferation–>INC translocation risk)}] = [Endemic_Africa (latent infection w/EBV) → Mandibular lesion] vs [Sporadic_USA → abd/pelvis lesion]

Histo =

“Starry Sky appearance”
[Diffuse mid-sized lymphocytes with interspersed macrophages (arrows)
basophilic cytoplasm
and high [Ki-67 fraction-proliferation index]

Answer 321

A

binds Fc portion of [IgE⼀antigen complex] → cross-links → degranulation^{(releases histamine, heparin and eosinophil chemotaxis factors)}
mediates allergic reaction / [Type 1 hypersensitivity]
[Cromolyn sodium (asthma px)] prevents mast cell degranulation

Answer 322

A

auto recessive; [HgB electrophoresis^{( will show HgbS with NO_HgbA)}] determines carrier status

[GlutaMATE –> Valine @ 6th position of the [β-chain globin]

Answer 323

A

1.Sickle Cell Anemia (INC Fetal HgbF synthesis)
2.AML ⼀^{(Rapidly ⬇︎WBC)}
3.[CML_{with blast crisis} (Chronic Myelogenous Leukemia w/blast crisis)]⼀^{(Rapidly ⬇︎WBC)}

Inhibits [Ribonucleotide Reductase] –> inhibits [DNA thymine] synthesis

Answer 324

A

[A- or B- Mothers] have mostly [anti-Rh IgM antibodies]–IgM does NOT cross placenta

[TYPE O ^-MOTHERS] HAVE MOSTLY [anti-Rh IgG antibodies] –IgG crosses placenta! –> HDN^EF

Answer 325

A

a. enteric bacteria synthesizes [oxidized_inactive vitamin K] ( this means neonates will not have Vitamin K and need px!)
b. [oxidized_inactive vitamin K] is [reduced⼀activated] by [epoxide reductase _{(inhibited by Warfarin)}] → [reduced_ACTIVATED vitamin K]
c. [_reduced__ACTIVATED vitamin K] acts as cofactor for maturing _factors[2,7,9,10,C,S] during synthesis which → [^(2,7,9,10)Pro_2ºCoagulation] and [^{(Protein C,S)}Anticoagulation(EARLY Warfarin☠️)]
—————

☠️: [^{(Protein C,S)}Anticoagulation* are *(EARLY Warfarin Victim☠️)] ➜ 1st to ⬇️ when Warfarin inhibits epoxide reductase = IMPORTANT SINCE ALLOWS FOR 1 WEEK/TEMPORARY UNINHIBITED → [^(2,7,9,10)Pro_2ºCoagulation] -➜ = [Warfarin induced skin necrosis]

Answer 326

A

anti

_________________

1-{[endothelial cell thrombin-thrombomodulin complex]} activates [Protein C]

2-[activated Protein C] uses [Protein S] to [cleave ( = inactivate)] 5a and 8a of coagulation cascade

Answer 327

A

During [Primary hemostasis platelet plugging] vs lab diagnostics,

Ristocetin activates [vWF ^{(which is already bound to subendothelial collagen exposed from injury})] to bind to [Gp1b_platelet aDherence R]

Answer 328

A

[Erythrocyte Sedimentation Rate] is used because [Acute-phase reactants (i.e. fibrinogen)] cause RBC to aggregate → higher density than plasma → [⇪ RBC Sedimentation]

_________________

infections
SLE
RA
temporal arteritis
malignant CA
Ulcerative Colitis IBD
Pregnancy

Answer 329

A

[Erythrocyte Sedimentation Rate] is used because [Acute-phase reactants (i.e. fibrinogen)] cause RBC to aggregate → [RBC-aggregates] have higher density than plasma → [⇪ RBC Sedimentation]

_________________

polycythemia
Sickle Cell Anemia
CHF
microcytosis
hypOfibrinogenemia

Answer 330

A

“Discern {[EBR^{[Echinocyte/Burr=Renal🌀]} _from ASL^{[Acanthocyte/Spur(ky)=Liver🌀]}] _{⼀red blood cells}}!”

_________________

[Acanthocyte Spur_ky RBC] =
1. [L_{iver🌀 ^{:Liver Disease}] or
2. [Cholesterol❌^{:abetaLipoproteinemia cholesterol dysregulation}}]

[Acanthocyte Spur RBC] are Spurky = Spiky!

Answer 331

A

[Schistocyte helmet RBC]

_________________

DIC
TTP
HUS
[traumatic hemolysis^{(i.e. mechanical heart valve )}]

Answer 332

A

[Spherocyte RBC]

_________________

Hereditary Spherocytosis
G6PD deficiency
autoimmune hemolysis

Answer 333

A

[Macro-ovalocyte (macrocyte) RBC]

_________________

Megaloblastic anemia ^(am_FOB)
Nonmegaloblastic anemia^(an_LAR)

Answer 334

A

[Ringed sideroblast _inRBC]

_________________

Sideroblastic anemia^{(pathologic excess iron in mitochondria)}

Answer 335

A

[Teardrop RBC]

_________________

1º Myelofibrosis

^{(bone marrow infiltration → forces RBC out of bone marrow → tear shape)}

Answer 336

A

[Bite RBC]

_________________

G6PD deficiency

^{(RBC oxidation of hgb sulfhydryl groups ^{< 2/2 loss of G6PD buffer system >} → [denatured hgb precipitation (AKA Heinz bodies)]. [Spleen macrophage Phagocytic damage] of these [Heinz bodies] →RBC membrane damage → [Bite}^RBC^]

Answer 337

A

[howell Jolly bodies _inRBC]

_________________

Spleen❌ ^{(functional hypOsplenia/asplenia)}

^{(basophilic nuclear remnants in RBC that are usually removed by spleen macrophages)}

Answer 338

A

[Heinz bodies _inRBC]

_________________

G6PD deficiency

^{(oxidation of hgb sulfhydryl groups → [denatured hgb precipitation (AKA Heinz bodies)]. [Splenic macrophage Phagocytosis] of these [Heinz bodies] →RBC membrane damage → [Bite}^RBC^{]^{(and after so many bites → unstable Spherocyte RBC)})}

Answer 339

A

[Basophilic stippling _ofRBC]

_________________

“_Basi_cally, ACid alcohol is Le-Thal

Anemia of Chronic Disease
alcohol abuse
Lead poisoning
Thalassemia

Answer 340

A

[Target RBC]

_________________

“HALT! said the LIVid hunter to his target”

HbC
Asplenia
LIVER disease
Thalassemia

Answer 341

A

“PVS is IDA as IEA”

[iron deficiency anemia ^{(microcytosis, hypOchromia)}] that manifest as …

⼀Iron deficiency anemia

⼀Esophageal webs

⼀Atrophic glossitis

Answer 342

A

[Normal Adult Hgb (Hgb A)] =

[4 globin chains: (α₂ β₂)] =

^globin:[< 2 x α^{(chromo 16: 2 alleles per 1 globin)} > + < 2 x β^{(chromo 11: 1 allele per 1 globin)} >] =

^alleles: [^{chromo 16}<αα / αα > + ^{chromo 11}<β / β >]

Answer 343

A

★ → defect in ALAS of heme synthesis →[isolated elevated iron^{(specifically in mitochondria)}] → [Bone Marrow Ringed sideroblast RBC (that contain iron-laden mitochondria)] ➜
★ [⇪ iron / ⇪ FerriTin / nl_TIBC]

★ [X-linked],
★ [acquired (myelodysplastic syndromes)],
★ {reversible (BAIL Out the Copper) with [Pyridoxine B6 (cofactor for ALAS) tx]}

Answer 344

A

[HgbA gene point mutation causes [Glutamic acid → Valine] at [position 6 of the β chain monomer] = HgbS =
[DICK/DeOxygenation] of HgbS → [CAP-_{(crystallization aggregative polymerization)}] → [HgbSS|SC Sickle Shaped RBC].
Will Un-sickle once O2 is bound again but eventually → RBC Membrane stiffness →
a. Chronic Hemolytic Anemia
- Intravascular hemolysis 2/2 membrane instability
- Extravascular hemolysis 2/2 red pulp splenic sequestration of sickles → ultimately causes splenic hypoxia/fibrosis → [auto/functional splenectomy]
b. Small Vessel Occlusion by sickles → Vasoocclusive Pain Crisis
c. Aplastic Crisis (2/2 Parvo B19 ⬇︎ erythroid precursors)
d. [Sickle RBC = ⬇︎1/2 life] → Anemia
HgbF is protective

Answer 345

A

Preferential vasodilation of arteriole–>increased capillary hydrostatic pressure–>increased fluid movement into interstitium

Answer 346

A

*dana *

antidsDNA (indicates and tracks development of lupus nephritis)

Answer 347

A

[anti-platelet Ab^{(against platelet_Gp2b/3A)}] start binding to [Platelet R 2b/3A] = forms [Antibody/Platelet complex] (no obvious cause > precedes viral/HIV?HCV? infxn)
_________________
→ splenic macrophages removes [Ab/Platelet complex] from circulation ➜ [isolated thrombocytopenia <100K]
_________________
- → superficial/mucosal bleeding
- [⇪ megakaryocytes on bone marrow biopsy]
_________________
-NORMAL SPLEEN
-normal clotting factors
-normal clotting PT/aPTT

Strongly associated with HIV and HCV

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