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CAIS - Review Flashcards

Unit 1

1
Q

What is the definition of heart failure?

A

Cardiac output unable to meet O2 demands of the body.

Or

Can only meet demands with increased filling pressure.

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2
Q

What is the formula to calculate blood pressure?

A

Blood Pressure = cardiac output X total peripheral resistance

or

BP = stroke volume X heart rate X total peripheral resistance

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3
Q

What is the formula to calculate cardiac output?

A

CO = stroke volume X heart rate

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4
Q

What are three determinants of BP?

A

Volume
The generating force
Resistance

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5
Q

If CO = SV X HR, what does this mean?

A

CO = amount of blood circulating per minute.

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6
Q

What is the formula to calculate stroke volume?

A

SV = end diastolic volume - end systolic volume

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7
Q

What is the formula to calculate ejection fraction?

A

ejection fraction = SV / EDV

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8
Q

Stroke volume is affected by what?

A

Contractility, Afterload, and Preload

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9
Q

What causes an increased stroke volume?

A

Increase in contractility
Increase in preload
or
Decrease in afterload

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10
Q

A failing heart will have an (increase/decrease) in stroke volume?

A

A decrease in stroke volume.

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11
Q

What are three general causes of heart failure?

A
  1. Myocardial Impairment
  2. Sudden preload increase
  3. Impaired ventricular filling
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12
Q

What are some causes of myocardial failure?

A
  1. Ischemic heart disease
  2. cardiomyopathies
  3. chronic hypertension
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13
Q

Chronic hypertension leads to _____ which will then lead to myocardial failure.

A

Ventricular remodeling

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14
Q

Post MI, what is a likely cause of sudden AV valve regurgitation?

A

Papillary muscle rupture

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15
Q

Infectious Endocarditis can cause sudden regurgitation of what heart valve?

A

Aortic valve

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16
Q

A papillary muscle rupture and infectious endocarditis will suddenly (increase / decrease) the preload.

A

Increase

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17
Q

What are three conditions that impair ventricular filling?

A
  1. constrictive pericarditis
  2. cardiac tamponade
  3. mitral and/or tricuspid valve stenosis
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18
Q

Papillary muscle rupture usually occurs how many days after a myocardial infarction?

A

2-7 days

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19
Q

Which valve is most likely to suffer from severe regurgitation from a post MI papillary muscle rupture?

A

Mitral valve

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20
Q

Bacterial endocarditis - the acronym FROM JANE stands for what?

A 
Fever
Roth Spots
Osler Nodes 
Murmur 
Janeway Lesions 
Anemia 
Nail-bed hemorrhage 
Emboli
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21
Q

What is the difference between osler nodes and janeway lesions?

A

Osler nodes are tender raised lesions on finger and toe pads.

Janeway lesions are small, painless, erythematous lesions on the palm or the sole.

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22
Q

Small hemorrhages (splinter like) underneath the nail bed raise concern for what kind of infection?

A

Bacterial Endocarditis

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23
Q

Round white spots on the retina surrounded by hemorrhage are referred to as what? What condition is this seen in?

A

Roth spots and Bacterial Endocarditis

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24
Q

Compression of the heart by fluid (blood / effusions) in the pericardial space resulting in a decrease in cardiac output is referred to as what?

A

Cardiac Tamponade

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25
Q

Define pulsus paradoxus.

A

Pulsus paradoxus is a decrease in amplitude of systolic blood pressure by >10mmHg during inspiration.

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26
Q

Pulsus paradoxus is commonly seen in what two cardiovascular disorders?

A

Caridac tamponade and pericarditis

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27
Q

Classically cardiac tamponade presents with the Beck Triad, what is the Beck Triad?

A

Beck Triad = hypotension, distended neck veins, and distant heart sounds.

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28
Q

Systolic heart failure is categorized as ______ and diastolic heart failure is categorized as ______.

A

Systolic heart failure is categorized as “Heart Failure with reduced Ejection Fraction” and diastolic heart failure is categorized as “Heart Failure with preserved Ejection Fraction.”

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29
Q

Systolic Heart Failure = pump failure = failure to contract.

What are some causes for this?

A

Ischemic heart disease and dilated cardiomyopathy

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30
Q

Diastolic Heart Failure = Filling Failure = Failure to relax

What are some causes for this?

A

Chronic hypertension and hypertrophic cardiomyopathy

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31
Q

Parallel hypertrophy is considered (concentric or eccentric)?

A

Parallel hypertrophy is considered concentric.

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32
Q

Would you expect to see cardiomegaly on a CXR for concentric hypertrophy?

A

No, concentric hypertrophy has parallel inward thickening.

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33
Q

Serial hypertrophy is considered eccentric hypertrophy is caused by a direct response to what?

A

Eccentric hypertrophy is caused by a direct response to volume overload.

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34
Q

Eccentric (serial) hypertrophy would be considered normal in what kind of patient?

A

An athlete

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35
Q

What is the most common cause of right sided heart failure?

A

Left sided heart failure

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36
Q

Left sided heart failure can cause pulmonary venous congestion, pulmonary edema, and poor perfusion to the organs.

What would you expect to find on the CXR due to the pulmonary edema?

A

Pulmonary edema from Left sided heart failure CXR finding:

vascular congestion
cephalization
Kerley B lines

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37
Q

What physical exam findings would you suspect for right sided heart failure?

A

Jugular vein distention
Hepatojugular Reflux
RUQ fullness / distention
Pitting edema

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38
Q

Left Atrial pressure is normally 5-10mmHg, as pressure increases what kind of findings would you suspect to develop?

A
  1. Cephalization (10-15mmHg)
  2. Kerley B Lines (15-20mmHg)
  3. Pulmonary Interstitial edema (20-25mmHg)
  4. Pulmonary Alveolar Edema (>25mmHg)
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39
Q

How does the renal system react is response to a decrease in cardiac output?

A

Renal system activates the renin–angiotensin–aldosterone system, which produces more angiotension II, which increases total peripheral resistance.

This helps maintain blood pressure levels.

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40
Q

A prolonged decrease in cardiac output will cause a prolonged activation of RAAS. These patients will most likely present with (hypertension or hypotension)?

A

Hypertension

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41
Q

Edema depends on what two variables?

A

Hydrostatic pressures and oncotic pressure

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42
Q

Ischemic heart disease, hypertension, cardiomyopathy, valvular disease, and pericardial disease are all common etiologies for what umbrella term?

A

Heart Failure

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43
Q

What condition is usually secondary to valvular disease and a less common cause of primary heart failure?

A

Heart Arrhythmia

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44
Q

A nucleated biconcave cell that carries O2 to tissues and CO2 to the lungs.

A

Erythrocytes

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45
Q

What is the average life span of a human erythrocyte?

A

120 days

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46
Q

Erythrocytosis (polycythemia) will have an increase of what on a CBC?

A

An elevated hematocrit

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47
Q

Red blood cells that vary size is referred to as what? What will be elevated on the CBC?

A

Anisocytosis with an elevated RDW

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48
Q

Platelets are derived from what precursor?

A

Megakaryocytes

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49
Q

The majority of platelets (1/3) are stored in what organ?

A

The spleen

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50
Q

Platelets interact with what protein to form a platelet plug?

A

Fibrinogen

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51
Q

Granulocytes and agranulocytes are considered what type of blood cell?

A

Leukocytes (white blood cells)

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52
Q

What is the percent differential count for the following white blood cells?

Neutrophil 
Lymphocyte 
Monocyte 
Eosinophil 
Basophil
A 
Neutrophil - 60%
Lymphocyte - 30%
Monocyte - 6%
Eosinophil - 3%
Basophil - 1%
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53
Q

Acute inflammatory response cell, phagocytic, multilobed nucleus, and numbers greatly increase during bacterial infections.

A

Neutrophil

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54
Q

Hypersegmented neutrophils are seen in a deficiency of?

A

Vitamin B12 and Folate deficiency

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55
Q

During bacterial infections or patients with CML, the peripheral smear will show an increase of what?

A

Band Cells (immature neutrophils)

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56
Q

Large kidney-shaped nucleus cell that differentiates into macrophages in tissues.

A

Monocyte

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57
Q

Phagocytose bacteria, cellular debris, and senescent RBCs.

Examples include: Kupffer cells, histiocytes, Langerhan cells, osteoclasts, and microglial cells.

A

Macrophages

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58
Q

Bilobed nucleus packed with large granules of uniformed size.

Defends against helminthic (parasite) infections and high phagocytic for antigen-antibody complexes.

A

Eosinophil

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59
Q

Causes of eosinophilia can be remembered with the acronym PACCMAN, what does PACCMAN stand for?

A

PACCMAN

Parasites 
Asthma 
Churg-Strauss Syndrome 
Chronic adrenal insufficiency 
Myeloproliferative disorders 
Allergic Processes 
Neoplasia (Hodgkin Lymphoma)
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60
Q

Densely packed granule cell that mediates allergic reactions.

A

Basophils

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61
Q

Another cell that mediates against allergic reactions and comes from the same precursor as basophils.

A

Mast Cells

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62
Q

Category that includes B cells, T cells, and NK cells.

A

Lymphocytes

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63
Q

What is the composition of fetal and adult hemoglobin?

A 
Fetal hemoglobin (HbF) = 2 Alpha and 2 Gamma
Adult Hemoglobin (HbA) = 2 Alpha and 2 Beta

Remember:

Alpha Always; Gamma Goes; Becomes Beta

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64
Q

Acanthocytes are also called what?

A

Spur Cells

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65
Q

Spur cells are associated with what kind of disease?

A

Liver Disease

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66
Q

On a peripheral smear in a patient with sideroblastic anemia, what would you expect to see?

A

Basophilic stipping and ringed sideroblasts.

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67
Q

Basophilic stippling is associated with what kinds of pathology?

A

Sideroblastic anemia (lead poisoning) and thalassemia.

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68
Q

Thalassemia could cause several changes on the peripheral blood smear, what are they?

A

Basophilic stipping
dacrocytes (tear drop cells)
target cells

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69
Q

G6PD Deficiency Patients will have these two changes on a peripheral smear.

A

Degmacytes (bite cells) and Heinz Bodies

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70
Q

How do you differentiate a burr cell from a spur cell?

A

Burr cell projections are more uniformed and smaller.

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71
Q

Echinocytes (burr cells) are in what kind of pathology?

A

End-stage renal disease
Liver disease
Pyruvate Kinase Deficiency

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72
Q

Megaloblastic Anemia will show these on a peripheral smear.

A

Macro-ovalocytes

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73
Q

Hemolytic anemias may show schistocytes on a peripheral smear, what is another name for schistocytes?

A

Helmet Cells

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74
Q

Sickle cell anemia patients may have sickled RBCs present, what are some reasons for the presence of sickle cells?

A

Dehydration
Deoxygenation
High Altitude

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75
Q

A small spherical RBC without the normal central pallor is referred to as?

A

A spherocyte

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76
Q

Spherocytes are seen in patients with?

A

Drug and infection inducted hemolytic anemias.

It can also be hereditary.

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77
Q

What are the four MAIN causes for target cells?

A

HbC Disease
Asplenia
Liver Disease
Thalassemia

HALT said the hunter to the Target

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78
Q

Patients with function hyposplenia or asplenia will have what on a peripheral smear?

A

Howell-Jolly Bodies

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79
Q

Microcytic anemia is classified as having an MCV value lower than?

And list at least 3 different types of microcytic anemias.

A

MCV < 80 fL

Different types of microcytic anemias: 
Iron Deficiency (most common)
alpha-Thalassemia
beta-Thalassemia 
Lead Poisoning 
Sideroblastic Anemia
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80
Q

RBC formation is called?

A

Erythropoiesis

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81
Q

Adult hematopoiesis occurs where?

A

The bone marrow.

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82
Q

What type of iron is found in adult Hemoglobin?

A

Ferrous Iron (2+)

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83
Q

Where does heme synthesis occur in the cell?

A

The mitochondria

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84
Q

Where does globin syntheis occur in the cell?

A

The cytoplasm

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85
Q

What are the normal percentages for hemoglobin types in an adult patient?

A

Hgb A = 98%
Hgb A2 = 2%
Hgb F = <1%

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86
Q

Hgb S is found in patients with what disease?

A

Sickle Cell trait/disease

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87
Q

Iron is bound and transported in the blood by what protein?

A

Transferrin

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88
Q

Transferrin transport most of the iron to the bone marrow, where what occurs?

A

Hemoglobin synthesis

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89
Q

Where is iron stored within the body?

A

In the liver bound to ferritin.

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90
Q

What substance improves the absorption of iron?

A

Ascorbic acid (orange juice)

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91
Q

Iron is not cleared well from the body, it is generally eliminated by sloughed enterocytes in stool or from bleeding.

Therefore iron overload is toxic, over does needs what form of treatment?

A

Chelation treatment

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92
Q

What form is iron in when it binds to transferrin?

What protein puts iron into this state?

A

Ferric state (3+)

Ferroxidase Protein oxidizes Fe2+ to Fe3+

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93
Q

What are the three primary values for a CBC?

A

RBC count, Hgb, and Hct

Remember the rule of 3’s

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94
Q

Define MCV

A

Mean Corpuscular Volume

volume / size of the RBC

95
Q

Define MCH

A

Mean corpuscular Hgb (mean cell Hgb)

content or weight per RBC

96
Q

Define MCHC

A

Mean corpuscular Hgb Concentration.

Reveals concentration and color per RBC

This value should not be increased.

97
Q

Define RDW

A

Red Cell Distribution Width

size and uniformity

Anisocytosis = size variability
Poikilocytosis = shape variability
98
Q

Explain TIBC

A

TIBC = Total Iron Binding Capacity

This value reflects the number of unbound transferrin, or the empty seats.

99
Q

What is serum ferritin?

A

Reflects the level of iron bound to ferritin and stored.

100
Q

What is transferrin saturation?

A

The percentage of iron bound to transferrin.

101
Q

When would you use hemoglobin electrophoresis?

A

To diagnose different hemoglobinpathies (sickle cell, thalassemia, etc).

102
Q

List at least four causes of macrocytic anemia.

A 
B12 Deficiency 
Inherited 
GI Disease or Surgery 
Folic Acid Deficiency 
Alcoholism 
Thiamine Responsive 
Reticulocyte miscount
Endocrine 
Dietary 
Chemotherapy 
Erythrocyte decrease
Liver disease
Lesch-Nyhan syndrome
Splenectomy
103
Q

List at least two normocytic anemias.

A

Aplastic anemia
Anemia of Chronic Disease
G6PD Deficiency
Sickle Cell Disease

104
Q

There are four major pathology categories for abnormal hemoglobin synthesis.

Name them and provide an example for each.

A
  1. Globin Chain Qualitative Problem: Sickle Cell Disease
  2. Globin Chain Quantitative Problem: Thalassemia
  3. Heme Synthesis Problem: Porphyrias
  4. Iron not incorporated normally into the Heme: Sideroblastic
105
Q

Valine is substituted for glutamic acid on what chain causes sickle cell disease?

A

The beta chain

106
Q

Hgb S Polymerization occurs when?

A

When there is an increased demand for O2 from the tissues, leading to an increase in O2 release from the RBCs.

107
Q

Infection, Decreased pH, Temperature changes, Dehydration, high altitude, and overexertion are all triggers for?

A

A sickling episode in a patient with sickle cell disease.

108
Q

Describe the Bohr Effect

A

O2 dissociates from Hgb more readily when the pH is lowered.

Increased O2 demand due to increased metabolism.
Increased metabolism = more CO2 = lower intracellular pH
H+ loads onto Hbg and O2 unloads = sickling

109
Q

There are several complications in sickle cell disease.

Name at least two.

A
  • Aplastic Crisis
  • Autosplenectomy
  • Splenic Infarct
  • Osteomyelitis
  • Painful Crises
  • Sickling in renal medulla
110
Q

Why is hydroxyurea used for treatment in patients with sick cell disease?

A

Hydoxyurea increases Hbg F production, thus reducing the chance of a sickling crisis.

111
Q

What are some complications from a painful crisis in a patient with sickle cell disease?

A

Painful crisis = vaso-occlusion

This leads to dactylitis, priapism, acute chest syndrome, avascular necrosis, and possible stroke.

112
Q

What is “crew cut” ?

A

Crew cut skull can be seen on xray due to marrow expansion from increased erythropoiesis.

This is seen in sickle cell and Thalassemia patients.

113
Q

Sickle cell anemia decreases immunity. Poor cellular flow leads to decreases in what?

A

Decreased:

  • WBC delivery
  • O2 delivery
  • Tissue support and repair
114
Q

Sickle cell trait is protective against what kind of parasite and related disease?

A

Sickle Cell Trait is protective against Plasmodium Invasion, therefore reducing risk of a malarial infection.

115
Q

How does the sickle cell trait for protection against malaria work?

A

The Plasmodium invasion produces intracellular hypoxia, this causes the cells to sickle, phagocytes respond and rid the body of the abnormal cells with the parasite.

116
Q

Acute chest syndrome is caused by pneumonia, infection, and sickling red cells.

It can be hard to determine the difference in the cause of ACS, so how is treatment decided?

A

Patient is generally treated for both infection and sickling cells.

Infections are treated with antibiotics and sickling is treated with a blood transfusion.

117
Q

Leg ulcers are commonly seen in patients with sickle cell disease, what are the common causes for this leg ulcers?

A

Leg ulcers in sickle cell patients are commonly caused by insect bites or cuts that fail to heal. This is due to poor blood circulation to the skin.

118
Q

A normal red blood cell’s life span is about 120 days. What is the average life span for a red cell in sickle cell anemia?

A

About 10-20 days.

119
Q

The reticulocyte count in sickle cell anemia will be increased or decreased?

A

Increased

120
Q

Define plasia

A

Formation or development

121
Q

Define metaplasia

A

cellular transformation

122
Q

Define dysplasia

A

Disordered cellular transformation

123
Q

Define Neoplasia

A

Irreversible

124
Q

List out malignant progression in order

A
  1. Metaplasia
  2. Dysplasia
  3. Neoplasia
125
Q

Define Hyperplasia

A

Increase in cell number

126
Q

Define Hypertrophy

A

Increase in cell size (muscle cell or fiber)

127
Q

The esophagus has what kind of cellular lining?

A

Nonkeratinized stratified squamous epithelium

128
Q

List the three embryonic gut regions.

A

Foregut, Midgut, and Hindgut

129
Q

What structures are found in the foregut?

A

Pharynx, lower esophagus to proximal duodenum, liver, gallbladder, pancreas, and spleen.

130
Q

What structures are found in the Midgut?

A

Distal duodenum to proximal 2/3 of transverse colon.

131
Q

What structures are found in the Hindgut?

A

Distal 1/3 of transverse colon to upper portion of the rectum.

132
Q

A condition where the epithelium in the distal esophagus changes from stratified squamous to columnar cells.

A

Barrett’s Esophagus

133
Q

Barrett’s Esophagus is caused by what other GI condition?

A

Chronic gastroesophageal reflux disease (GERD)

134
Q

Barrett’s esophagus increases a patients risk for what?

A

Esophageal adenocarcinoma

135
Q

List the three types of pain discussed during the GI review lecture.

A
  1. Somatic Pain
  2. Visceral Pain
  3. Referred Pain
136
Q

What are two GI disorders we commonly associate with having referred pain?

A
  1. Appendicitis (epigastric region)

2. Cholecystitis (right shoulder pain)

137
Q

What is a visceral ligament?

A

Visceral ligaments attach organs to the body wall or another organ. Typically this ligaments will have a rich nerve supply.

138
Q

McBurney’s Point tests for what?

A

Appendicitis

139
Q

Describe the progression of appendicitis.

A

Periumbilical pain that migrates to the RLQ of the abdomen. Nausea and Fever and usually present. Peritonitis is expected on physical exam.

140
Q

How do you differentiate between an upper and lower GI bleed?

A

Bleeds above the ligament of Treitz is an upper GI bleed and below the ligament are a lower GI bleed.

141
Q

A disorder in which the lower esophageal sphincter fails to relax and a “birds beak” appearance on radiograph.

A

Achalasia

142
Q

What are two compounds produced by the stomach parietal cells?

A

Intrinsic factor and Gastric Acid

143
Q

What is intrinsic factor used for?

A

Intrinsic factor is a B12 binding protein that is required for the uptake of B12 at the terminal ileum.

144
Q

Where is gastrin produced?

A

In the G cells of the antrum of the stomach and duodenum.

145
Q

Gastrin stimulates the production of what?

A

Gastric Acid

146
Q

D cells of the pancreatic islets and GI mucosa produce what major regulatory substance?

A

Somatostatin

147
Q

Chief cells located in the stomach produce what? What is this product used for?

A

Pepsin, which aids in protein digestion.

148
Q

Name the three enzymes produced by the pancreas for macronutrient digestion.

A 
alpha-amylase = starch/polysaccarhide digestion
Lipase = fat digestion 
Protease = protein digestion
149
Q

Gallstones are caused by what gallbladder disorder?

A

Cholelithiasis

150
Q

What are the four F’s for cholelithiasis?

A

Female
Fat
Fertile
Forty

151
Q

Name and describe the two types of stones seen in cholelithiasis.

A

Cholesterol stones: 80% of stones and opaque due to calcifications.

Pigment Stones: black, radiopaque

152
Q

How is cholelithiasis diagnosed?

A

Using ultrasound.

153
Q

Cholelithiasis is a gallstone, so what is choledocholithiasis?

A

Choledocholithiasis is the presence of a gallstone in the common bile duct. This condition leads to an elevated ALP, GGT, direct bilirubin, and/or AST/ALT levels.

154
Q

Cholecystitis is defined as?

A

Acute or chronic inflammation of the gallbladder.

155
Q

Name the three types of cholecystitis.

A
  1. Calculous cholecystitis (most common)
  2. Acalculous cholecystitis
  3. Gallstone Ileus
156
Q

Choledocholithiasis can lead to inflammation of what neighboring organ?

A

The pancreas, causing pancreatitis.

157
Q

What is the triangle of Calot?

A

It is a surgical landmark made up of the cystic duct, common hepatic duct and the cystic artery.

158
Q

What is the triangle of Calot important?

A

As a surgical landmark, it helps the surgeon identify the cystic artery for ligation during a cholecystectomy.

159
Q

Define ascending cholangitis.

A

A bacterial infection of the biliary tract (common bile duct) originating from the duodenum. The bacteria move up the bile duct causing inflammation, this is usually secondary to some type of obstruction within the bile duct.

160
Q

What is Charcot’s Triad?

A

Used for ascending cholangitis

  1. Jaundice
  2. Fever
  3. RUQ Pain
161
Q

What is Reynold’s Pentad?

A

Also used for cholangitis
Reynold’s Pentad is Charcot’s Triad (jaundice, fever, RUQ Pain) +

Mental Status Change and Shock (hypotension)

162
Q

In hemorrhagic pancreatitis what are two signs you suspect to see?

A

Cullen’s sign (periumbilical bleeding) and Grey Turner Sign (flank bleeding)

163
Q

Where is Traube’s space?

A

Left - Mid Axillary Line 6 ICS

164
Q

Where is Castell’s Sign?

A

Left - Anterior Axillary Line Lowest ICS

165
Q

What are the two most common causes of peptic ulcer disease?

A

H. pylori infection and NSAIDS

166
Q

An ulcer associated with pain during meals and weight loss?

A

Gastric Ulcer

167
Q

What are three complications of having a peptic ulcer?

A
  1. Hemorrhage
  2. Obstruction
  3. Perforation
168
Q

Duodenal ulcers usually cause pain during or after eating?

A

Patients may find relief of pain while eating, but the pain can return a few hours after consuming a meal.

169
Q

Gastroesophageal Reflux Disease (GERD) commonly presents with what symptoms?

A

Heartburn, regurgitation, and dysphagia. Patient may also complain of having a cough.

170
Q

A condition where the stomach herniates upward through the esophageal hiatus of the diaphragm.

A

Hiatal Hernia

171
Q

What is the most common type of hiatal hernia?

A

A sliding hiatal hernia, also referred to as an hourglass stomach.

172
Q

What are the two major liver enzymes seen on a Liver Function Test?

A

Alanine Transaminase (ALT) and Aspartate Transaminase (AST)

173
Q

Besides ALT and AST, what are two other lab values one can order to access liver function?

A

Alkaline Phosphatatse (ALP) and gamma-Glutamyl Transferase (GGT)

174
Q

Micronodular nodular growth on the liver indicates what kind of etiology?

A

Alcohol or hemochromatosis

175
Q

Macronodular nodular growth on the liver indicates what kind of etiology?

A

Chronic viral hepatitis

176
Q

Virchow’s node (left-sided supraclavicular lymph node) is a sentinel lymph node for cancer and can denote metastasis. What is this sign called when Virchow’s node it enlarged and hard?

A

Troisier’s Sign

177
Q

What are the two primary veins that conjoin and make up the portal vein?

A

The splenic vein and the superior mesenteric vein

178
Q

A portal triad consists of what?

A

A hepatic artery, hepatic portal vein, and a hepatic duct. (Lymph and nerve innervation runs with portal triad too)

179
Q

The portal branches of the portal vein take blood to the ______ to then be absorbed by the hepatocytes.

A

Sinusoids to be absorbed by the hepatocytes

180
Q

Hepatic veins drain directly into what major venous vessel?

A

The inferior vena cava

181
Q

The portosystemic system consists of what three major veins and the portal vein.

A

The splenic vein, the inferior mesenteric vein, and the superior mesenteric vein.

182
Q

The common bile duct and the pancreatic duct conjoin to form what structure?

A

The hepatopancreatic ampulla (ampulla of vater)

183
Q

The spleen separates RBCs into Heme and Globin. Heme interacts with the enzyme heme oxygenase to become what compound?

A

Biliverdin

184
Q

Biliverdin is converted into unconjugated bilirubin by biliverdin reductase. Unconjugated bilirubin is lipid or water soluble?

A

Lipid soluble

185
Q

What protein transports unconjugated bilirubin to the liver?

A

Albumin

186
Q

Unconjugated bilirubin interacts with the enzyme UGT to be converted into Conjugated Bilirubin, which is soluble in?

A

Conjugated bilirubin is water soluble

187
Q

After bilirubin is conjugated and it is secreted what are the three things that can happen to it?

A

Excreted via urine as urobilinogen
Recycled via enterohepatic circulation
Excreted via feces as stercobilin

188
Q

Indirect Hyperbilirubinemia is most commonly caused by?

A

Hemolysis

189
Q

Direct Hyperbilirubinemia is most commonly caused by?

A

Biliary tract Disease or biliary obstruction

190
Q

Antibodies are produced by what lymphocyte?

A

B lymphocytes

191
Q

B lymphocytes produce several different immunoglobin classes:

  • IgA
  • IgD
  • IgE
  • IgM
  • IgG

Which one means a patient was previously exposed to the antigen?

A

IgG

192
Q

A patient with a Acute Viral Hepatitis A, with no previous exposure, would be expected to have what positive lab finding?

A

+ anti-HAV IgM

193
Q

A person who was vaccinated for Hep A would be expected to have what positive lab finding?

A

+ anti-HAV IgG

194
Q

A patient that has tested positive for HBsAg within the past 6 months ( <6 months ) has what disease?

A

Acute Hepatitis B

195
Q

Hepatitis B is considered chronic when?

A

A patient has tested + for HBsAg for more than 6 months

196
Q

A patient has a + HBeAg, this would indicate what?

A

A patient with chronic HBV with high levels of virus within the hepatocytes.

197
Q

What lab values would you expect to see for patient with a past exposure to HBV that was resolved?

A
  • HBsAg
    + anti-HBs IgG
    + anti-HBc IgG
198
Q

Someone who was immunized against the HBV would have what positive lab finding?

A

+ anti-HBs IgG

199
Q

Hepatitis D can only infect patients with past or current exposure to what disease?

A

Hepatitis B

200
Q

Elevated AST and ALT values where the AST is double the amount of ALT is indicative of what disorder?

A

Alcoholic Hepatitis

201
Q

ALT and AST values of > 3000IU is seen in what kind of situation?

A

Toxic injury due to drugs/medications

202
Q

Acute hepatitis usually shows AST and ALT levels between what two values?

A

AST and ALT will generally be between 500-3000 IU

203
Q

Ammonia in the body comes from where?

A

Broken down amino acids

204
Q

Explain how ammonia is metabolized in a healthy liver.

A

Ammonia is absorbed by the GI tract, it is transported in the portal blood to the liver, the liver converts ammonia into urea, the urea enters systemic circulation and enters the kidneys, finally the urea is excreted via urine.

205
Q

What is the most common reason for build up of ammonia in the body?

A

Portal hypertension, the ammonia is unable to enter the hepatocytes to be metabolized.

206
Q

When ammonia is allowed to build up and enter other cells of the body what condition can eventually develop?

A

Hepatic Encephalopathy.

207
Q

What is the primary treatment for hepatic encephalopathy?

A

Lactulose - converts ammonia (NH3+) into ammonium (NH4+) which is then excreted in the feces.

Patient should also be treated with an antibiotic (rifaximin) to reduce ammonia producing gut bacteria.

208
Q

What are signs and symptoms of ammonia toxicity?

A
  • Disorientation
  • asterixis
  • difficult to arouse
  • coma
  • overall mental confusion
209
Q

What is asterixis?

A

A flapping tremor of the hands

210
Q

A condition that shows macrovesicular fatty changes in the liver and may be reversible with alcohol cessation.

A

Hepatic Steatosis

211
Q

Intracytoplasmic eosinophilic inclusions of damaged keratin filaments are more commonly referred to as?

A

Mallory bodies

212
Q

In alcoholic hepatitis which value is generally greater, AST or ALT?

A

AST > ALT (ration is usally > 2:1)

213
Q

What is the final and irreversible form of alcoholic liver disease?

A

Alcoholic cirrhosis

214
Q

In alcoholic cirrhosis, regenerative nodules surrounded by fibrous bands are in response to what?

A

Chronic liver injury, portal HTN, and end-stage liver disease.

215
Q

In nonalcoholic fatty liver disease which lab value is greater AST or ALT?

A

ALT > AST

216
Q

Nonalcoholic fatty liver disease is suspected in patients would are?

A

Suffering from metabolic syndrome (insulin resistance) and who are obese.

217
Q

What is a classic lab finding in a patient with primary biliary cholangitis (cirrhosis)?

A

+ anti-mitochondrial antibody and increase in IgM

218
Q

This disease is an autoimmune reaction leading to lymphocytic infiltrate and granulomas, and eventual destruction of lobular bile ducts.

A

Primary Biliary Cholangitis (Cirrhosis)

219
Q

Primary Biliary Cholangitis is most commonly seen in what patient population?

A

Middle-aged Women

220
Q

Alternating strictures and dilation with beading of intra- and extrahepatic bile ducts on ERCP is classic for this disease.

A

Primary Sclerosing Cholangitis

221
Q

Primary Sclerosing Cholangitis is most commonly seen in what patient population?

A

Middle-aged men with IBD

222
Q

Primary Sclerosing Cholangitis is most common associated with what disorder?

A

Ulcerative Colitis

223
Q

Primary Sclerosing Cholangitis increases at patients risk for what type of cancer?

A

Cholangiocarcinoma and gallbladder cancer

224
Q

A positive anti-smooth muscle lab finding indicates what disease?

A

Autoimmune hepatitis type 1

225
Q

What is the most common primary cause of a malignant tumor of the liver in adults?

A

Hepatocellular Carcinoma

226
Q

Hepatocellular Carcinoma is strongly associated with what other disease?

A

Hepatitis B Virus (and other forms of cirrhosis)

227
Q

Hepatocellular cancer may lead to this syndrome.

A

Budd-Chiari Syndrome

228
Q

How is hepatocelluar cancer diagnosed?

A
  1. +alpha-fetoprotein lab
  2. ultrasound or contrast CT/MRI
  3. Biopsy
229
Q

What lab values will be severly elevated in acute pancreatitis?

A

Serum amylase and lipase (up to 3x the normal limit)

230
Q

A patient would is a long time alcoholic, with diabetes, and a history of steatorrhea is at risk for?

A

Chronic Pancreatitis

231
Q

Pancreatic Cancer is most common in what part of the pancreas?

A

The head of the pancrease

232
Q

Describe Courvoisier Sign

A

Obstructive jaundice with palpable, nontender gallbladder.

233
Q

What is the treatment of choice for a patient with confirmed Pancreatic Adenocarcinoma of the head of the pancreas?

A

The Whipple Procedure

234
Q

Risk factors for pancreatic cancer include:

A
  • Tob use
  • Chronic Pancreatitis
  • Diabetes
  • Age >50
  • Jewish or African-American

PA (4 decks)

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