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Medical Diagnosis > Lecture 9 (Lab)-Exam 4 > Flashcards

Lecture 9 (Lab)-Exam 4 Flashcards

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USMLE® Step 1 flashcards
1
Q

Coagulation cascade:
* What is it?
* Why is it activated?
* What is the first step? (2)
* What are the pathways?

A
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2
Q

Extrinsic pathway
* When is it activated?
* What does it involve?

A
  • Becomes activated secondary to external trauma
  • Involves initiation by factor III (Tissue factor- found in cells membranes) and its interaction with factor VII
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3
Q

Intrinsic Pathway
* Responds to what?
* What factors?

A
  • Responds to spontaneous, internal damage of the vascular epithelium
  • Involves factor XII, XI, IX, and VIII
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4
Q

Common Pathway
* What is it?
* What are the factors?

A
  • Both intrinsic and extrinsic pathways meet at a shared point to continue coagulation
  • Involves factors X, V, II (Thrombin), I (Fibrin), and XIII
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5
Q

The extrinsic and intrinsic pathway both lead into what? ⭐️

A

the final common pathway by independently activating factor X

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6
Q
  • Factor I, in the context of blood coagulation, is also known as what?
  • Fibrinogen is what?
  • When blood vessels are injured, fibrinogen is converted into what? By what?
A
  • Factor I, in the context of blood coagulation, is also known as fibrinogen.
  • Fibrinogen is a glycoprotein that is essential for blood clot formation.
  • When blood vessels are injured, fibrinogen is converted into fibrin by the action of thrombin, and this fibrin forms a mesh that traps blood cells, resulting in a clot. Therefore, factor I (fibrinogen) plays a crucial role in the coagulation cascade
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7
Q
  • Hepatocytes are responsible for providing the body with what?
  • Clotting factor III (tissue factor) originates from what?
A
  • Hepatocytes are responsible for providing the body with clotting factors XIII, XII, XI, X, IX, VII, V, II, and I
  • Clotting factor III (tissue factor) originates from endothelial cells, whereas clotting factor VII is freely available in plasma
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8
Q
  • Vitamin K dependent factors are what? What is needed?
  • Vit K assists in what?
  • Vitamin K is what?
  • Warfarin therapeutic effects are negated by what?
A
  • Vitamin K dependent factors – 2, 7, 9, 10 – need calcium to be activated
  • Vit K assists in the carboxylation of clotting factors II, VII, IX, X, protein C and S
  • Vitamin K is a lipid soluble vitamin
  • Warfarin therapeutic effects are negated by the administration of fresh frozen plasma and vitamin K (takes longer)
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9
Q

Protein c and s

  • What is protein C and S? Where are they made?
  • In protein C or protein S deficiency the coagulation cascade continues as what? What is it caused by?
  • Patients with this condition are prone to what?
A
  • Protein C and S are glycoproteins, synthesized in the liver and are Vit K dependent
  • In protein C or protein S deficiency the coagulation cascade continues unchecked with overactivity of Factor V and factor VIII resulting in excessive thrombin production
    * Caused by inherited gene mutations (missense mutation most common 60-70%) or acquired from liver disease, medications, malignancies
  • Patients with this condition are prone to thromboembolic events such as DVT/PE, stroke
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10
Q

Protein C and S
* How do you test?
* Can also do what?
* What is the txt? Important to do what?

A
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11
Q
  • Warfarin inhibits what?
  • What is the half life of protein C and S? When it is inhibited?
A
  • Warfarin inhibits Vit K dependent clotting factors and protein C and S
  • Protein C and S have short half life and are inhibited first when coumadin administered which further promotes the procoagulant effect of other Vit K factors and forms microthrombi
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12
Q

THE END RESULT OF THE COAGULATION CASCADE

Fibrin
* What is fibrin?

A

Fibrin is a long, thin protein with branches produced at the end of the coagulation cascade when fibrinogen (factor 1) is converted to fibrin, which stabilizes the blood clot

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13
Q

Cryoprecipitate
* Cryoprecipitate is used to what?
* Cryoprecipitate is rich in ?
* Used to treat what?
* Cryoprecipitate can be used as second-line therapy for what?

A
  • Cryoprecipitate is used to control bleeding related to fibrinogen deficiency. It is a small volume of 10 to 20 mL per unit
  • Cryoprecipitate is rich in fibrinogen, fibronectin, clotting factors VIII and XIII, and von Willebrand factor.
  • Used to treat low fibrinogen levels in **post operative patients or critically ill patients **
  • Cryoprecipitate can be used as second-line therapy for von Willebrand disease and hemophilia A (factor VIII deficiency), but appropriate individual clotting factors should be considered first.
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14
Q

Coagulation testing-Prothrombin time (PT)
* PT – measures what?
* PT is measured in time -normal time is what?

A
  • PT – measures coagulation throughout the extrinsic pathway and the common pathway
  • PT is measured in time -normal time is between 11-15 seconds, but varies based on the healthcare setting
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15
Q

INR (International normalized ratio):
* What is it used for?
* PT can be prolonged with what?
* Therapeutic INR differs based on what?

A
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16
Q
  • PTT – measures what?
  • What is the normal time?
  • Test of choice when monitoring a patient on what?
  • What is aPTT?
  • If abnormal it could indicate abnormality in what?
A
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17
Q

Coagulation testing-D-Dimer
* After healing, the clot is no longer needed and the body uses what?
* The fragments of the disintegrating fibrin are called what?
* One of the final fibrin degradation products produced is what?
* The level of D-dimer in the blood can significantly rise when?

A
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18
Q

What are the results of the d-dimer test?

A
  • Negative means that it is highly unlikely that a thrombus is present.
  • Positive only means that more testing needs to be carried out for clots, (ex: ultrasound,CT angiography )
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19
Q

Hemophilia
* What type of disease? What are the two types?
* Will present with what?

A

Hemophilia A(Classic hemophilia) is an x-linked recessive coagulopathy that results in dysfunctional VIII and Hemophilia B (Christmas disease) is a deficiency in Factor IX
* Both factors are involved in the activation of factor X which is a key step in conversion of prothrombin to thrombin and then thrombin converting fibrinogen to fibrin

Will present with easy bruising, bleeding after dental procedures or surgery

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20
Q

Hemophilia
* Can treat with what? (2) What is the MOA?

A

Can be treated with desmopressin and recombinant factor VIII
* Desmopressin causes endothelial cells to release vWF as well as factor VIII from where it is stored in the tissue
* Hemophilia B (Christmas disease) is an X-linked recessive coagulopathy that results in dysfunction of IX

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21
Q

Hemophilia causes prolonged what?

A

Both diseases will cause prolonged PTT, the difference is hemophilia A is a cofactor deficiency while hemophilia B is a protease deficiency
* Hemophilia A and B will have a normal PT/INR

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22
Q

Von Willebrand disease (vWF)
* What type of disease?
* What is vWF?
* Since vWF increases the half life of VIII you can expect to see what?
* What is the txt?

A
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23
Q
  • What is are the different types of vwd?
  • What is the von willebrand panel?
A
24
Q
  • The effects of vitamin K deficiency can be observed in both where?
  • Can be seen in patients with what?
A
  • The effects of vitamin K deficiency can be observed in both the extrinsic and intrinsic pathways and directly measured via PT and PTT
  • Can be seen in patients with poor diet, pancreatic insufficiency, liver disease, intestinal flora imbalances
25
Q

Vitamin K in infants
* Newborns are given what?
* What is the main source of vit K?
* Child presents with what?- Most likely what? ⭐️

A
  • Newborns are given a single dose of intramuscular vitamin K injection after birth as their guts are sterile
  • Gut bacteria are the main source of vitamin K in humans apart from dietary intake
  • Child presents with lethargy, refusal to feed, bulging fontanelle – most likely interventricular hemorrhage
26
Q

Platelet dysfunction
* What are the Indications for platelet function testing include? (3)

A
  • Unexplained bleeding with negative initial evaluation.
  • Positive family history of a platelet function disorder.
  • Genetic test results that suggest a platelet function disorder.
27
Q

The initial evaluation that typically precedes platelet function testing includes:
* Thorough history of what?
* What labs? (2)
* What screening tests?

A
  • Thorough history of bleeding challenges, using a bleeding assessment tool (BAT), and family history of bleeding disorders.
  • Complete blood count (CBC) with platelet count and examination of the peripheral blood smear.
  • Standard coagulation testing with prothrombin time (PT) and activated partial thromboplastin time (aPTT).
  • Screening tests for von Willebrand disease (may be omitted in some cases)
28
Q
  • What is the gold standard for platelet testing?
  • how does it work?
A
29
Q

P2Y12:
* What is it?
* What are drugs?

A
  • the platelet P2Y12 receptor for ADP plays a central role in platelet function, hemostasis, and thrombosis
  • Drugs such as Plavix (clopidogrel) inhibit the P2Y12 receptor and are potent antithrombotic drugs – however this is only adequate in about 1/3 of patients – ticagrelor (Brilinta) and prasugrel (Effient) are more efficacious
30
Q

What is TEG (Thromboelastometry?

A
  • A non-invasive test that quantitatively measures the ability of whole blood to form a clot
  • Performed in a specifically designed system called a thromboelastograph
  • Measures the functional ability of the blood to make a hemostatic plug
31
Q

What is PFA (Platelet function assay)?

A
  • aggregate in consequence of agonist presence in the system
  • The time taken by platelets to occlude the orifice in the test which is an overall measure of platelet-related hemostasis
32
Q
  • What are troponins?
  • What are the three types and where are they found?
  • When damage or death of cardiac tissue occurs, what is released?
A
33
Q
  • Troponin is attached to what?
  • In the event of myocardial damage, what is released first?
  • What else is released?
  • Traditional troponin begins to rise when?
  • What test is able to be detectable sooner?
A
34
Q

High sensitivity troponin
* What is it?
* What can it measure?
* Must have what?
* Troponin is tradionally ordered how?

A
35
Q

What is stable angina, unstable angina, NSTEMI, STEMI?

A
36
Q

Natriuretic peptides (NP’s) are what?
* What do they regulate?
* Used as a biomarker for what?
* BNP is expressed predominantly by what?

A

Natriuretic peptides (NP’s) are key proteins that improve and regulate circulation
* They regulate blood pressure, inhibit cardiac hypertrophy and remodeling
* Is used as a biomarker for congestive heart failure

BNP is expressed predominantly by cardiomyocytes

37
Q

When is BNP released?
* In a normal heart the main site of BNP expression is in where?
* Helps the body do what?
* Guides what?

A

When there is ventricular distention/myocardial muscle stretching, it is released by those cardiac cells
* In a normal heart the main site of BNP expression is in the atrial regions – ventricular BNP gene expression increases drastically in cardiac diseases affecting the ventricles, like in heart failure
* Helps the body compensate for HF promotes urine excretion, relaxes blood vessels, and lowers BP
* Guides diagnoses and treatment of congestive heart failure

38
Q
  • What is BNP?
  • NT-proBNP Is more sensitive for what?
  • An abnormal BNP result would trigger what?
  • There is evidence of a linear relationship with increasing BNP levels and what?
A
39
Q

ckmb
* What is it?
* What are the different types and where can they be found?

A

Creatinine kinase is an enzyme that catalyzes the reversible phosphorylation of creatinine by ATP
* CKBB – found in central nervous system (brain)
* CKMM- found in adult skeletal muscle
* CKMB – found in myocardium (1-2% in skeletal too)

40
Q

CK-MB is elevated with what?

A

with injury to cardiac muscle, BUT may also see transient increase with rhabdomyolysis, myocarditis, intense exercise, and trauma

41
Q

CK-MB was used as a criteria for diagnosing acute MI (1980-1990’s)
* What was the issue?
* First appears when?
* When does it peak and stays how long?
* Usually undetectable levels when?
* Reported as positive if greater than what?

A
42
Q

What is CRP?
* What is it induced by?
* What can it activate?

A

CRP is a protein synthesized by the liver, whose level rises in response to inflammation
* Acute phase reactant protein that is induced by the IL-6 action during the acute phase of an inflammatory/infectious process
* It can activate the classic complement pathway and activate phagocytic cells

43
Q

CRP levels rise and fall rapidly with what?
* Persistently elevated CRP levels can be seen in who?
* Markedly elevated levels of CRP are most often associated with what?

A
  • CRP levels rise and fall rapidly with the onset and removal of the inflammatory stimulus
  • Persistently elevated CRP levels can be seen in chronic inflammatory conditions
  • Markedly elevated levels of CRP are most often associated with an infectious cause
44
Q

C-reactive protein (crp)
* can be used for what?
* What are the different levels

A
45
Q

What are the general interpretations of CRP levels? (5)

A
  • Less than 0.3 mg/dL: Normal (level seen in most healthy adults).
  • 0.3 to 1.0 mg/dL: Normal or minor elevation (can be seen in obesity, pregnancy, depression, diabetes, common cold, gingivitis, periodontitis, sedentary lifestyle, cigarette smoking, and genetic polymorphisms).
  • 1.0 to 10.0 mg/dL: Moderate elevation (Systemic inflammation such as RA, SLE, or other autoimmune diseases, malignancies, myocardial infarction, pancreatitis, bronchitis).
  • More than 10.0 mg/dL: Marked elevation (Acute bacterial infections, viral infections, systemic vasculitis, major trauma).
  • More than 50.0 mg/dL: Severe elevation (Acute bacterial infections). 90% of the time
46
Q

C-reactive protein crp
* False elevation caused by what?
* Mild elevations in CRP can be seen without what? Who has a higher level of CRP?

A
  • False elevation caused by: Certain medications, such as non-steroidal anti-inflammatory drugs (NSAIDs), Statins, recent injury or illness, Magnesium supplementation

Mild elevations inCRPcan be seen without any systemic or inflammatory disease.
* Females and elderly patients have higher levels ofCRP. Obesity, insomnia, depression, smoking, and diabetes can all contribute to mild elevations inCRP, and the results shall be interpreted with caution in individuals with these comorbidities

47
Q
  • Lipid panel includes what?
  • In addition to a routine lipid panel, it is possible for the clinician to measure a number of other parameters including what?
A
  • Lipid panel includes: LDL, HDL, total cholesterol, triglycerides
  • In addition to a routine lipid panel, it is possible for the clinician to measure a number of other parameters including apolipoprotein B and A-I levels, LDL and HDL size, LDL and HDL particle number, and lipoprotein (a) (Lp(a)) levels
48
Q

Indication for testing lipids:
* Patient with what type of history? (2)
* Patients whith what?
* Risk stratification for patients?

A
49
Q

Cholesterol
* What is it?
* Crucial for what?
* New research suggests that individuals living with moderately high cholesterol for a long time who have HTN may have the same risk of heart disease as who?

A
  • Cholesterol is a sterol compound found in most human body tissues
  • Crucial for cell membranes and metabolic processes in the body – used to make hormones, fat-soluble vitamins, and bile acids
  • New research suggests that individuals living with moderately high cholesterol for a long time who have HTN may have the same risk of heart disease as those who have high cholesterol for only a short time
50
Q

How is cholestoral classifed based on its density?

A
  • High-density lipoprotein (HDL)
  • Low-density lipoprotein (LDL)
  • Very-low-density lipoprotein (VLDL) – carry triglycerides which is the fat your body stores up and uses for energy between meals
51
Q

HDL
* _ cholesterol?
* Absorbs what?
* The liver than does what?
* High levels can lower what?

A
  • “Good” cholesterol
  • Absorbs cholesterol in the blood and carries it back to your liver
  • The liver then flushes it from the body
  • High levels can lower your risk for heart disease and stroke
52
Q

LDL
* makes up most of what?
* It can build up where?
* If you have extremely high LDL levels you may notice what?
* LDL is comprised of three subclasses of what? Which one is most damaging?

A
53
Q

Lipoprotein-a or Lp(a) – high levels may mean what?

A

you are at a high risk of heart disease even if your other cholesterol levels are healthy – your genes code for this, the level is unlikely to change much from childhood to adulthood

54
Q

What is xanthoma? what is corneal arcus?

A
55
Q

Triglycerides
* What is it?
* Comes from what?
* How many adults have high triglycerides?
* High blood triglycerides that stay higher than 175 mg/dL for a long time can raise what?
* Very high blood triglycerides (>500 mg/dL) – can raise the risk for what?

A

Medical Diagnosis (16 decks)

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