CM - Fall Final 2n1s

basophilic stippling

lead poisoning

what does lead poisoning affect?

CNS

macrocytic anemia

BAD HL

• B12 deficiency

• Alcoholism 

• Hypothyroidism

• Down syndrome 

• Liver disease

what are RBC abnormal inclusions?

• reticulocytes

• howell-jolly bodies

• basophilic stippling

• heinz bodies

• nucleated RBC (blasts)

reticulocytes

ribosomal RNA

howell-jolly body

DNA chromatin remnants

basophilic stippling is associated with?

ribosomes at edge of cells

heinz bodies

denatured Hb

when are heinz bodies seen?

g6pd def

Nucleated red blood cells (NRBCs or erythroblasts) in peripheral blood comes out d/t?

BM (Bone marrow) stress

what is WBC inclusion

dohle bodies

dohle bodies

 light, blue-gray, oval basophilic inclusions in neutrophils

b12 vs. b9 (folate): peripheral neuropathy

B12 (CNS issues)

microcytic anemia

TAILS

• Thalessemia 

• Anemia of Chronic Disease/Illness 

• Iron deficiency

• Lead poisoning

• Sideroblastic anemia

H/H ratio

1/3 ratio

nail spooning

iron def anemia

what does TIBC measure?

transferrin levels

hemostasis (coagulation)

first step in all wound healing. Wounds can’t heal until bleeding stops.

when does intercranial hemorrhaging occur?

PLTS <20k/microliter

von willebrand’s disease

Most common hereditary coagulation abnormality

factor V leidan mutation

Most common hereditary thrombophilia

PTT

intrinsic pathway → VIII, IX, XI, XII (8 9 11 12)

PT

extrinsic pathway → Tissue Factor (III), VII (3, 7)

best way to know a patient’s clotting

ask history - do you bleed/bruise easily?

3 clotting factors not made in liver

Factors III (Tissue Factor), IV (Calcium), and VIII

vit-k dependent clotting factors and anticoags

• clotting factors— 2, 7, 9, 10

• Anticoagulants— proteins C, S, Z

fibrinogen

factor I

prothrombin

factor II

reed-sternberg cells (owl eyes)

hodgkin’s lymphoma

auer rods*

acute myeloid leukemia (AML)*

lysosomes and their crystalized contents

philadelphia chromosome*

CML*

smudge cell

CLL

what immune system do you need to have inflammation?

INNATE

CH4

Th (t helper cells)

what does innate immune system defend against?

novel infection onsets

innate immunity

this is the first time you’re seeing new Ag.

This is slow bc B cells must first be activated by TH cell and proliferate BEFORE it can have an effective immune response.

image of 2 abnormal cells seen with a smear of lead poisoning. what do the RBC inclusions represent?

residual ribosomal RNA (rRNA)

(the blue dots = basophilic stippling)

increased amounts of fibrinogen and globulins in plasma result in this lab finding

rouleaux formation

the osmotic fragility test is useful in detecting what?

hereditary spherocytosis

Spherocytes have reduced surface area–to–volume ratio.

They are less able to tolerate hypotonic solutions, so they lyse earlier than normal RBCs → inc osmolarity

when reviewing a list of RBC indices on the report of patient’s CBC, a report of MCV (mean corpuscular volume) is sufficient on its own to satify you that the patient’s RBC are normal size

false

what is in one molecule of hemoglobin?

4 heme units and 4 globin chains

what are the granulocytes?

neutrophils, eosinophils, basophils

what is the most abundant component of plasma?

albumin

acute phase reactants

• might be explained in part by diversion of AA toward synthesis of crucial portein catalysts

• mediates responses to stress ie fever, leukocytosis, thrombocytosis, and increased cortisol

what system is the acute phase reactants part of?

considered part of the innate immune system

acute phase reactants

substances that change in plasma concentration by >25% in response to inflammatory chemical mediators

most abundant cell in bloodstream

erythrocytes

if patient has clubbing of nails, they most likely have anemia caused by a def of what?

iron

in the question, whose serum contains anti-A and anti-Rh antibodies, but no anti-B antibodies?

B-

what immunoglobulin can cross the placenta?

igG

what is a cause of hypochromic, microcytic anemia?

lead poisoning

Alcohol causes what kind of anemia?*

macrocytic anemia*

folic acid def causes what kind of anemia?

macrocytic/megaloblastic anemia.

acute blood loss causes what kind of anemia?

usually normocytic, normochromic anemia initially

what cell pattern would result in normal MCV and elevated RDW? ((Mean Corpuscular Volume) (Red Cell Distribution Width = distribution in size)

mixed microcytosis and macrocytosis

RDW

measures the differences in width of RBCs

a 38 y/o male presents to ER with 2 week history of non-bloody diarrhea that has progressive gotten worse. he has minimal urine output and is admitted for dehydration. his stool specimen is positive for parasites. what WBC would be elevated?

eosinophills

the 4 children have A, O, B, and AB blood types. the phenotype of the couple must be what?

A and B (AO and BO)

what are some causes of macrocytic anemia?

• alcoholism

• b12/folate acid def

• liver disease

• down syndrome

(NOT LEAD POISONING → microcytic)

what are the causes of pernicious anemia?

antibodies directed against intrinsic factor

antibodies against gastric parietal cells that make it

what can elevated serum levels of methylmalonic acid (MMA) indicate early def of what?

B12

a patient has less RBC, low Hgb, RDW, low iron, low transferrin saturation, low reticulocytes, high ferritin?

anemia of chronic illness

anemia of chronic disease because inflammation traps iron in storage (high ferritin) and suppresses erythropoiesis (low reticulocytes), despite low serum iron

what is the mechanisms where gastrectomy causes megaloblastic anemia?

no parietal cells → reduced intrinsic factor production, which is needed for absorption of B12 → b12 deficiency → megaloblastic anemia

a pt when hemophilia A (factor VIII def) would have abnormalities in what lab test of clotting?

aPTT only (intrinsic)

schistocytes are most likely to be found on blood smears of patients suffering from what?

TTP (microangiopathic hemolytic anemia (MAHA))

why does ITP not have schistocytes?

immune platelet destruction → only thrombocytopenia

NO schistocytes because hemolysis is not microangiopathic

TTP is a microangiopathic hemolytic anemia with thrombocytopenia, fever, neurologic symptoms, and renal involvement due to ADAMTS13 deficiency/ultra-large vWF multimers

what factors are integral to the EXTRINSIC pathway of coag?

factor III and VII

what is true about primary (Cellular hemostasis)?

it results in temporary blockage of a break in the wall of a blood vessel by plt plug

vit-k dependent clotting factors are part of what hemostasis?

secondarily

when does primary hemostasis start?

primary hemostasis begins immediately (within seconds)

what is most accurate and complete list of thrombophilias inherited in an autosomally dominant pattern?

protein C deficiency,

protein s def,

antithrombin (III) def,

factor V leidan mutation

chronic ITP (immune thrombocytopenia)

• prior episode of acute ITP is not required

• symptoms last 12 months

• 2-3x more common in F than M

• more common in adults

• there is a tendency for chronic ITP to recur often

LMWH (fractionated) has more ___ what activity than anti-factor IIa (anti-activated thrombin) activity?

anti-Xa activity

heparin undergoes a change in its properties when UFH is separated into chains of shorter and shorter length. what is the end result?

heparin’s ability to selectively activate antithrombin-mediated inhibition of factor Xa increases

opsonization

process where foreign invader is marked on surface to make it easier for phagocytic cells to recognize

what is derived from myeloid lineage of cells? name myeloid lineage vs. lymphoid lineage

• polycythemia rubra vera

• essential thrombocytosis

• lymphoma

(NOT myelogenous leukemia)

Myeloid lineage produces:

• Red blood cells (erythrocytes)

• Platelets (from megakaryocytes)

• Granulocytes: neutrophils, eosinophils, basophils

• Monocytes → macrophages/dendritic cells

Lymphoid lineage produces:

• B cells → plasma cells

• T cells → helper, cytotoxic, regulatory

• NK cells

what are examples of type IV hypersensitivity?

poison ivy dermatitis, contact dermatitis, PPD reaction

II: Autoimmune hemolytic anemia

I: anaphylaxis

complement components does what to the immune system?

augments/amplifies

what is complement components?

trigger of inflammation

provides one method of opsonization

serum proteins that play a key role in innate and adaptive immunity

are compliment components able to direct cell lysis on their own?

no

complement

• Complement does not directly recognize antigens like antibodies do.

• It’s a cascade of serum proteins activated by antigen–antibody complexes (classical), pathogen surfaces (alternative), or lectin binding, but complement proteins themselves don’t bind antigens directly.

what happens if there is a recurrence of infection in terms of adaptive response?

adaptive response is much better at responding (faster and more effective)

what activates the 2” immune responses?

memory t and b cells

when b cell is activated by a receptor, what happens?

becomes a dedicated B cell aka plasma cell (forever only makes that one Ab)

what is an example of type 3 hypersensitivity?

RA

what are the 4 types of hypersensitivity and which is the fastest?

Type 1 - anaphylactic (seconds to min

Type 2 - Ab-dependent cytotoxic  (min to hr)

Type 3 = immune complex  (hours)

Type 4 = delayed/cell-mediated (1-2 days) 

• I.e., PPD skin test

what do type 1 hypersensitivity need?

igE abs and memory B cells

what does type 4 hypersensitivity need?

no need for abs, but needs memory T cells

what is the role of B12?

• Raw material used in the production of RBCs in the bone marrow (DNA synthesis)

• Neurological function

• Hyper-homocysteinemia → atherosclerosis

what can be an indicator of chronic myelogenous leukemia?

acute gouty arthritis

what are the 9 CVD risk factors?

Heart Develops Differences Once Fatty Cupcakes Shrink My Arteries

• Hypertension*

• Dyslipidemia*

• Diabetes mellitus / Insulin resistance*

• Obesity → BMI 30+ (or waist  circumference >40M, >35 W)*

• Family History

• Cigarette Smoking

• Sedentary Lifestyle

• Microalbuminuria or estimated GFR < 30 ml/min 

• Age (older than 55 men, 65 women)

what are both causes and effects of chronic HTN?

kidney disease and PAD (Sx: claudication, sex dysfxn/ED)

when do yo uwant to start tx of HTN earlier?

• Syndrome X (metabolic syndrome)

  • Hyperlipidemia (TC, LDL)

  • Hypertension

  • high blood glucose

  • Abdominal Obesity

what is syndrome X?

meet 3 of the 5 following traits 

•  Abdominal Obese BMI30+ or 40+M or 35+ F

•  TC 150+

•  HDL < 40 men or <50 women

• FBS 100-125

• HTN 130/85+

• **still counts if you are medicated for any of these!!! 

what is the treatment for PAD?

ASA (antiplts)

what is the #1 cause for PAD?

cause: atherosclerosis

what is #1 risk factor for PAD?

smoking

s/sx of PAD?

• Hair loss

• Thick nails, skin thin/shiny, delayed cap refill, hyperpigmentation, skin/fat necrosis

what is fludrocortisone fxn?

• Increase electrolyte reabsorption+water retention

• Synthetic corisol/cortisone; a synthetic aldosterone agonist → supports keeping BP up and keeping pipes filled 

what is fludrocortisone a tx for?

Tx for elderly with postural (orthostatic) hypotension if the 3 below don’t work 

1. Stop meds that lead to it (diuretics, venodilaters, etc)

2. Avoid dehydration 

3. Compression stockings