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MT3 Flashcards

1
Q

which bones in adults are generally responsible for hemotopoiesis?

A

long bones

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2
Q

buffy coat

A

lies between the layer of plasma and the layer of RBCS when blood is centrifuged. Contains WBCs and platelets

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3
Q

RBCs circulate for ____ days

A

120

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4
Q

RBCs are recycled in ____

A

spleen

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5
Q

Hb consists of:

A

4 heme groups and 4 globins

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6
Q

Hb synthesis requires (4)

A

iron
vit B12
vit B6
folic acid

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7
Q

Platelets are also called

A

thrombocytes

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8
Q

Generally speaking, anemia means…

A

low blood

Hb is below normal levels

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9
Q

anemia may be associated with (3)

hint: 3 forms anemia can take

A

different appearance of Hb
Reduced number of RBCs
Structural abnormalities in RBCs

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10
Q

Anemia may be a consequence of (3)

A

decreased hematopoiesis
abnormal hematopoiesis
Increased loss or destruction of RBCs

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11
Q

Anemias due to decreased hematopoiesis resulting from bone marrow failure

A 
Aplastic anemia (bone marrow doesn't work)
Myelophthisic anemia (something replacing bone marrow)
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12
Q

Anemias due to decreased hematopoiesis can also be caused by deficiencies in which nutrients?

A

vit B12, folic acid (megaloblastic anemia)

Protein deficiency

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13
Q

An example of anemia caused by abnormal hematopoiesis

A

sickle cell anemia (genetic cause)

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14
Q

Anemia can be the result of increased loss and destruction of RBCs.

What are some signs of this? (4)

A
  • bleeding
  • intrasplenic sequestration
  • immune hemolysis
  • infections (malaria)
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15
Q

Aplastic Anemia

  • cause
  • what happens
  • results
A
  • Idiopathic, secondary
  • Bone marrow depleted of hematopoietic cells; consists only of fibroblasts, fat cells, scattered lymphocytes
  • Leads to anemia, leukopenia, thrombocytopenia.
  • Leads to uncontrollable infections, bleeding tendency, chronic fatigue, sleepiness, weakness
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16
Q

Which is the most common form of anemia?

A

iron deficiency anemia

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17
Q

Iron deficiency anemia

  • prevalence
  • appearance
  • Etiology
A
  • Most common form of anemia
  • hypochormic (pale red cells), microcytic (small red cells) anemia

Etiology:

  • Increased loss of iron
  • inadequate iron intake/absorption
  • increased iron requirements
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18
Q

Megaloblastic anemia is caused by:

A

deficiency of vitamin B12 or folic acid

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19
Q

Megaloblastic anemia caused by vit B12 deficiency occurs due to…

A

Pernicious anemia
lack of gastric intrinsic factor
atrophic gastritis

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20
Q

Megalobalstic anemia caused by folic acid deficiency occurs due to…

A

Inadequate intake in diet or malabsorption caused by intestinal disease

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21
Q

Megaloplastic anemia:

What does it lok like

A

Bone marrow is hypercellular, with numerous megaloblasts
Peripheral blood shows macrocytic anemia.
Neutrophils are hypersegmented (5+ nuclei)

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22
Q

Sickle Cell Anemia etiology

A

Substitution of glutamic acid for valine
Synthesis of abnormal beta chain of globin.
Most prevalent among african americans

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23
Q

Sickle Cell Anemia results in

A
  • Multiple infarcts in various organs (neuro, sharp pains in bones, sleep, extremities)
  • Hyperbilirubinemia, jaundice (bile stones)
  • Delayed neuro dev (can be avoided medically)
  • Cardiopulmonary insifficiency
  • Recurrent infections
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24
Q

Thalassemia

- etiology

A
  • genetic defect in synthesis of HbA resulting in reduced rate of globin chain synthesis.
    No abnormal Hb produced. Just a slower rate.
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25
Q

Thalessemia minor vs major

A

minor - just the thalessemia trait. Heterozygotes with mild, nonspecific symptoms and asymptomatic.

major - homozygots. Severe, serious disease. Develop antibodies.

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26
Q

Beta-thalessemia vs alpha-thalessemia

A

Reduced sythesis of beta chain vs alpha chain of globin

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27
Q

Thalessemia presentation

A
  • hypochromic (pale RBCs)
  • Splenomegaly, heosiderosis, heptomegaly
  • Compensatory hyperplasia of BM
  • Calvarium ‘crew-cute’ hair
  • Hyperbilirubinemia, jaundice
  • Chronic and slows growth in children
  • Intellectual development impaired
  • Cardiorespiratory insufficiency
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28
Q

Hemolytic Anemia is caused by

A

destruction of RBCs (hemolysis)

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29
Q

Intracorpuscular defects of hemolytic anemia

A

Defects within the cell.

  • Structural abnormalities, sickle cells, thalessemia, hereditary spherocytosis
  • Infection (malaria)
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30
Q

Extracorpuscular defects in hemolytic anemia

A
  • ANtibodies, infectious agents, mechanical factors

- Autoimmune hemolytic anemia, hemolytic disease of the newborn, transfusion reactions

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31
Q

symptoms of hemolytic anemia

A
  • anemia
  • compensatory RBC hyperplasia in BM
  • hyperbilirubinemia, jaundice
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32
Q

Immune mediated anemias

A

Mediated by antibodies that destroy RBCs.

  • Autoantigens, alloantigens, neoantigens
  • Might be a mismatched blood transfusion, hemolytic disease of the newborn, or autoimmune disease.
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33
Q

Polycythemia vera
What is it?
Primary vs secondary.

A

Increased number of RBCs
PRIMARY - prolif of hematopoietic stem cells / uncontrolled prod of RBCs

SECONDARY - Increased RBC volume as a result of increased bone marrow caused by increased EPO. Usually caused by prolongued hypoxia (high altitudes)

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34
Q

Polycythemia symptoms

A
  • hypertension
  • dark red, or flushed face
  • headaches, visual problems, neurologic symptoms
  • Splenomegaly
  • Hypercellular BM
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35
Q

4 leukocytic disorder

A

Leukopenia
Leukocytosis
Lymphoma
Leukemia

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36
Q

Leukopenia

A

Too few WBCs

  • Neutropenia: bacterial infections or drugs (closapine)
  • Lymphopenia: Some infections
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37
Q

Leukocytosis

Characterized by (1)
Types (4)
Symptoms (2)

A
  • Too many WBCs
  • Neutrophilia - bacterial infection
  • Eosinophilia - allergies, skin diseases, parasitic infections
  • Lymphocytosis - viral infections, chronic infections, some autoimmune
  • Splenomegaly lymphadenopathy
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38
Q

Plasma cell myeloma

A

Malignant disease of plasma cells; lots of antibodies produced.

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39
Q

Leukemias are

A

Malignant diseases involving WBCs or their precursors in BM.

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40
Q

Two categories of leukemias

A

Myeloid - neutrophil, eosinophil, basophil

Lymphoid - B or T cells only

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41
Q

Etiology of leukemia

A

Bone marrow becomes overrun with leukemia cells. More immature blood cells in peripheral blood.
Bone marrow isn’t working properly so RBCs, WBCs, and platelets aren’t made normally.
Leads to anemia, infections, and bleeding/difficulties clotting.

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42
Q

Acute Lymphoblastic Leukemia

  • prevalence
  • origin
  • pathology
  • treatment
  • prognosis
A
  • Most common leukemia in children
  • Almost always B cell origin
  • Massive infiltration of bone marrow, peripheral blood, bleeding into skin/internal organs
  • Chemo –> 90% cure
  • Higher incidence of developing other cancers + social issues from young illness
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43
Q

Acute Myelogenous Leukemia

  • origin
  • how many abnormal cells?
  • prognosis?
A
  • Clonal proliferation of myeloid precursors in BM
  • 20% abnormal cells (cytogenic abnormalities)
  • Death 6 months after onset without treatment.
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44
Q

Chronic Myelogenous leukemia

  • origin
  • pathology
  • phases
  • treatment
A
  • Philadelphia chromosome with BCR-ABL rearrangement
  • BM and peripheral blood overrun with neutrophils and their precursors
  • (1) chronic phase, (2) accelerated phase, (3) blast cells
  • treat with tyrosine kinase inhibitors
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45
Q

Chronic Lymphocytic Leukemia

  • origin
  • populations
  • diagnosis
A
  • Almost exclusively B cells
  • Most patients older than 50
  • Lymphocytes > 5000/mL for diagnosis
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46
Q

Lymphomas are…

A

lymphoid cell malignant diseases predominantly involving lymph nodes.

Malignant cells infiltrate lymph nodes, spleen, thymus, or bone marrow. May involve other organs.

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47
Q

Lymphomas generally metastasize to

A

brain or spleen

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48
Q

Lymphomas - age groups

A

Can affect any age group.

More common in adults, more aggressive inkids.

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49
Q

Two categories of lymphomas are:

A

Non-Hodkin’s Lymphoma (B, T, NK cells)

Hodgkin’s Lymphoma (B cells)

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50
Q

Non-Hodgkin’s Lymphomas (generally)

A
  • No benign lymphomas
  • Most have B-cell phenotype
  • All age groups (more common in adults, more aggressive in children)
  • Can spill over into blood and present as leukemia
  • Involve lymph nodes, BM, spleen, thymus, but can be of extranodal origin.
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51
Q

Diagnosis of Non-Hodgkin’s Lymphomas

A
  • Light microscopy
  • Ancillary techniques: immunochemo, flow cytometry, cytogenic analysis
  • Clinical features: lymph node/spleen/liver enlargement, systemic constitutional symptoms (FNW), extranodal tumor spread.
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52
Q

Follicular Lymphoma

  • prevalence
  • characterstics
A
  • Most common lymphoma in USA
  • Slow growing
  • Presents as long-standing enlargement of lymph nodes, mild constitutional symptoms
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53
Q

Diffuse Large-Cell Lymphomas

  • what do the cells look like?
  • Prognosis?
A
  • Most aggressive Non-Hodgkin’s Lymphoma
  • Tissue infiltrated by large lymphoid cells with irregular nuclear outlines, prominent nucleoli
  • Complete remission in 75% of patients
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54
Q

Burkitt’s Lymphoma

A
  • Highly malignant tumor of B-cells

- Extranodal masses more prominent than enlarged lymph nodes

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55
Q

Burkitt’s lymphoma: Endemic ariant

A

sub-saharan africa, children infected with epstein-barr virus experience mandible and soft tissue involvement
- Sporadic and endimic variants.
Most can be cured

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56
Q

Burkitt’s Lymphoma: Sporadic variant

A

Children and young adults most affected.

Abdominal masses

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57
Q

Hodgkin’s Lymphoma

  • Populations
  • histology
A
  • Bimodal age distribution: Peaks at 25 and 55

- REed-Sternberg cells: bilobed nucleus, prominent nucleoli with clear halo

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58
Q

Five types of Hodgkin’s Lymphoma

A
  1. Nodular sclerosing
  2. Lymphocyte predominant
  3. Lymphocyte rich
  4. Mixed cellularity
  5. Lymphocyte depleted.
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59
Q

Hodgkin’s Lymphoma: Clinical Features

A
  • Enlarged lymph nodes
  • ## Extranodal involvement, leukemic spread (rare)
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60
Q

Plasma Cell/Multiple Myeloma

  • populations
  • how it works
  • prognosis
A
  • Most patients >45
  • Malignant plasma cells proliferate in bone marrow
  • Punched-out holes/lytic lesions in calvaria vertebrae
  • Hypercalcemia (turn on osteoclast function)
  • Renal failure (too much antibody)
  • Anemia, leukopenia
  • Death <3-4 years after diagnosis
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61
Q

Plasma Cell/Multiple Myeloma:

Diagnosis based on… (4)

A
  • X-rays (lytic lesions)
  • Serum electrophoresis (monoclonal spike)
  • Bone marrow biopsy (neoplastic plasma)
  • Clinical presentation
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62
Q

Edema - what is it (simply)

A

Too much fluid in tissues

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63
Q

Components of blood

A

Water
Electrolytes
Cells: RBCs, WBCs, platelets
Proteins: albumin, coagulation proteins, others

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64
Q

Albumin

A

Maintains oncotic pressure
Made by liver
Important in transportation (steroids, bile salts, FAs etc)

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65
Q

Two main drivers of fluid across capillary walls:

A
  1. Capillary Hydrostatic pressure

2. Capillary Oncotic Pressure

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66
Q

Capillary Hydrostatic pressure

A

pressure from heart pumping and the weight of blood

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67
Q

Capillary oncotic pressure

A

Albumin normally stays inside the capillary; only water and electrolytes can freely cross.

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68
Q

Typical fluid movement across capillary walls, to tissues and then to lymphatic channels

A

At first the hydrostatic pressure drives fluid out.
Hydrostatic pressure decreases toward venous side, becomes less than oncotic pressure and fluid is returned to the capillary. Small amounts of fluid enter lymphatic channels

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69
Q

Pericytes

A

Vascular supportive cells that are on the outside of capillary walls

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70
Q

Flow in the lymphatic system from extremities

A

Extremities -> lymph nodes -> thorax -> thoracic duct / right lymphatic duct ->venous system

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71
Q

Flow through a lymph node

A

afferent lymphatic vessel -> subcapsular sinus -> efferent lymphatic vessel

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72
Q

Causes of LOCALIZED edema (3)

A
  1. Ischemia
  2. Infection
  3. Lymphatic obstruction
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73
Q

How does ischemia cause localized edema?

A

Irreversible cell injury -> lysed cells release mediators that promote capillary leakage.
Fluid leaves leaky capillaries, overwhelms lymphatics, and accumulates in tissues.

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74
Q

How does infection cause localized edema?

A

Neutrophils/WBCs release mediators that cause capillaries to get leaky.

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75
Q

Two examples of infection that cause edema

A
  1. IMPETIGO
  2. CROHN’S DISEASE: presents with dilated lymphatics in the ileum because they are trying to drain local edema caused by inflammation there.
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76
Q

How does lymphatic obstruction cause localized edema?

A

Normally, lymphatic system removed fluid from tissues and eventually drains into thoracic duct/right lymphatic duct to return to venous system.
Blockage or damage of a lymphatic vessel or node with cause edema in the area corresponding to it

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77
Q

Example of localized edema caused by lymphatic obstruction.

A

Breast Carcinoma Therapy:

  • Axillary lymph node dissection (for treatment and/or tumor staging)
  • Radiation
  • Arm edema results from surgical removal of axillary lymph nodes and radiation of axilla.
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78
Q

Two mechanisms by which capillaries can become leaky

A
  1. Endothelial cell retraction (in response to chemical mediators; reversible)
  2. Endothelial cell injury (more sever damage results in endothelial cell necrosis and detachment; not reversible)
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79
Q

Leaky capillaries allow for ______ to escape, and water to follow.

Hint: normally kept within capillaries

A

albumin

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80
Q

Causes of SYSTEMIC edema

A
  1. Heart failure
  2. Kidney Disease
  3. Liver failure
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81
Q

Heart failure - what is it (simply)

A

heart is unable to pump enough blood to adequately perfuse tissues

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82
Q

How does left heart failure result in systemic edema?

A

Pressure increases in pulmonary veins, building pulmonary hydrostatic pressure. Fluid enters lung tissue (usually at base of lungs).

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83
Q

What is a clinical red flag for systemic edema caused by left heart failure?

A

Pulmonary edema -> you can hear crackles with a stethascope at base of lungs

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84
Q

How does right heart failure cause systemic edema?

A

Pressure increases in vena cavae -> hydrostatic pressure increases in systemic capillary bed, causing fluid to enter systemic tissues (usually seen in legs).

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85
Q

Pitting edema

A

Pressing on skin will leave an indentation. A presentation of systemic edema caused by right heart failure.

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86
Q

Systemic edema caused by heart failure leads to fluid build up in the bottom of lungs and legs. This is due to what?

A

Gravity

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87
Q

How does kidney disease cause systemic edema?

A

Normal kidneys don’t allow albumin to cross the glomerular basement membrane.
Diseased kidneys allow albumin to be filtered and released in urine.
Albumin concentration in the blood gets too low, thereby decreasing oncotic pressure. Hydrosatic pressure stays the same, so fluid will not return to the capillaries and will accumulate in tissues.

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88
Q

How does liver failure cause systemic edema?

A

Liver isn’t producing enough albumin so oncotic pressure in systemic circulation drops. Hydrostatic pressure stays the same so fluid is driven out of capillaries and accumulates in tissues.

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89
Q

Two forms that liver failure can take

A

Liver failure can be (1) not producing enough albumin, or (2) not producing enough clotting factors.

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90
Q

thrombus

A

a blood clot

Composed of platelets and fibrin. Entraps RBCs and WBCs.

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91
Q

Thrombo-embolus

A

a piece of thrombus breaks off and travels elsewhere in the body.

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92
Q

Hypercoagulable state

A

Condition in which blood clots form very easily

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93
Q

Atrial fibrillation

A

Disease of the heart where the atria have irregular twitchings.

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94
Q

Hemostasis

A

= coagulation

The process of thrombus formation at site of blood vessel injury to make bleeding stop.

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95
Q

Three major components that control thrombus formation

A

Endothelial cells
Platelets
Coagulation cascade

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96
Q

Process of thrombus formation

A

Damage to endothelium causes platelets to adhere;
Platelets aggregate and form a plug at the site of injury;
Coagulation cascade: Thrombin cleaves fibrinogen into fibrin, which stabilizes the platelet plug;
Platelets and fibrin form thrombus. They form laminations (layers) and trap RBCs.

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97
Q

Where to platelets come from

A

Megakaryocytes in bone marrow produce platelets and release them into the blood. Platelets are tiny fragements of megokaryocyte cytoplasm.

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98
Q

Pathologic thrombi can be caused by (3)

A
  1. Endothelial cell injury
  2. Poor blood flow
  3. Hypercoagulable state
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99
Q

Causes of arterial thrombi

A
  1. Atherosclerosis - hardening of the arteries; thrombi can form on plaques and then can break off
  2. Atrial Fibrillation - Uncoordinated chaotic contraction of atria resulting in areas of irregular blood flow (vulnerable for thrombus formation)
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100
Q

How atrial fibrillation causes arterial thrombi

A

Uncoordinated chaotic contraction of atria resulting in areas of irregular blood flow (vulnerable for thrombus formation)

Thrombi can develop on surface of left atrial appendage. These thrombi can break loose, embolize and cause infarction.

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101
Q

Consequences of arterial thrombi (3)

A

Myocardial infarction
Cerebral infarction
Kidney infarction

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102
Q

Venous stasis

  • what is it?
  • where is it most common?
  • risk factors?
A

poor blood flow

  • most common in leg veins
  • immobilization is a risk factor (long distance air travel, surgery)
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103
Q

Causes of venous thrombi

A
  1. Venous stasis
  2. Cancer (hypercoagulable state)
  3. Pregnancy
  4. Inherited thormbophilia
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104
Q

Pregnancy - a cause of venous thrombi?

A

Pro-coagulent changes with pregnancy are part of preparation for delivery (prevent excess hemorrhaging)

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105
Q

Inherited thrombophilia

A

Hypercoagulable state that causes venous thrombi;

Genetic abnormalities in coagulation proteins;

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106
Q

Potential thromboembolic consequences of venous thrombi

A

pulmonary emboli - venous thrombi end up in the lungs when they break. Leads to pleural infarction.

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107
Q

SHOCK

A

Circulatory failure that results in poor tissue perfusion resulting in cellular hypoxia

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108
Q

Three types of circulatory failure (shock)

A
  1. Cardiogenic shock
  2. Hypovolemic shock
  3. Septic shock
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109
Q

Cardiogenic shock

A

Eg: myocardial infarction, other heart pathology

Tissues aren’t getting enough blood because of heart pump failure.

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110
Q

Hypovolemic Shock

A

Eg: Trauma (blood loss)

Tissues aren’t getting enough blood because there is not enough blood volume.

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111
Q

Septic Shock

A

Shock associated with systemic inflammatory response, usually infection;
Systemic inflam response causes vasodilation. Tissues don’t get enough blood because peripheral blood vessels are markedly dilated.

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112
Q

Complications of shock (2)

A
  1. Acute respiratory distress syndrome

2. Disseminated intravascular coagulation

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113
Q

Acute Respiratory Distress syndrome

A

A common complication of shock;
Damage to pulmonary capillary endothelium and alveolar epithelium causes edema to enter alveoli;
Damage secondary to many things;
Other causes: aspiration, pancreatitis, smoke/toxic gas inhalation;
ACUTE phase - alveolar edema;
Later phases - progression to hyaline membranes and thickened alveolar walls. Resolve to normal function.

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114
Q

Disseminated Intravascular Coagulation

A

Complication of shock;
Caused by excessive activation of coagulation and formation of thombi in microvasculature of the body;
Causes consumption of coagulation factors and platelets, which can then lead to bleeding in other parts of the body (brain, kidneys, GIT etc);

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115
Q

Bones in adults

A

206
12% body weight
10% replaced annually

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116
Q

Periosteum

A

outer layer of bone

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117
Q

cortical bone

A

outer bone layer

thick, strong

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118
Q

Medullary bone

A

Inner bone layer

reticular, lace-like, not as strong

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119
Q

Epiphysis

A

end of a long bone

associated with cartilage cap and joint

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120
Q

Metaphysis

A

contains the growth plate; changes radically during growth

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121
Q

Diaphysis

A

Central portion of long bone

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122
Q

The two kinds of bone formation

A

Endochondral ossification

Intramembranous ossification

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123
Q

Endochondral ossification

A
  1. Begins in the Reserve Zone.
  2. Chrondrocytes proliferate in the Proliferative Zone
  3. Hypertrophy Zone - condrocytes hypertrophy and die, leaving spaces for blood and osteoblasts to move in.
  4. Mineralization Zone.
  5. Medullary Bone.
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124
Q

Functions of bones (4)

A

Support muscles / facilitate movement;
Protect organs;
Site of BM (hematopoiesis);
Storage of Ca and phosphate;

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125
Q

Vitamin D controls…

A

Increased Ca absorption by intestine;
Resorption of Ca by kidney;
Storage of Ca and phosphate;

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126
Q

What can cause a vitamin D deficiency?

A

Lack of exposure to sunlight;
Inadequate intake;
Abnormal intestinal absorption;

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127
Q

Osteopenia (osteomalacia)

A

Decreased mineralization (calcification of bones)

  • Bones are soft, pliable
  • Increased fractures
  • Rickets (in children)
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128
Q

Rickets

A

Decreased ossification of new bone in growth plates with failure to grow, bone deformities, fractures

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129
Q

Osteoporosis

  • What is it?
  • What is the effect?
  • What causes it? Primary vs Secondary
A
  • Reduction of bone mass. Cortical and medullary bone are lost.
  • Fracture risk increases (commonly in vertebrae, hips, distal radius)

Often multifactorial

  • PRIMARY: Idiopathic (older age, menopause, lifestyle, low initial bone mass are risk factors)
  • SECONDARY: Due to an identifiable cause (hormone imbalance, dietary insufficiency, drugs, tumours, immobilization)
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130
Q

Complete fracture

A

through entire thickness of bone

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131
Q

Incomplete fracture

A

Partial thickness of bone affected

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132
Q

Simple fracture

A

just one fracture

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133
Q

Comminuted fracture

A

multiple fractures

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134
Q

Closed fracture

A

skin is intact

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135
Q

Compound fracture

A

skin has been broken (more likely to be infected)

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136
Q

Complicated fracture

A

infected fracture

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137
Q

Pathologic fracture

A

Due to abnormal bone (osteoporosis, tumour)

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138
Q

The process of fracture healing

A
  1. HEMORRHAGE: Blood fill the gap left by fracture, and clots
  2. GRANULATION TISSUE: Inflam cells, fibroblasts, and new capillaries use blood clot framework to ingrow
  3. Soft tissue is transformed into WOVEN BONE
  4. As bone matures, and is subject to physical stress / weight-bearing, remodeling occurs
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139
Q

Granulation Tissue

A

Blood clot with invasion of new vessels and inflammatory cells. This is the second stage of fracture healing.

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140
Q

Woven Bone

A

Disorganized, swirling
Unlike mature bone, which has clear grain along mechanical forces
This is what soft (granulation) tissue is transformed into in the third phase of fracture healing.

141
Q

Osteomyelitis

A

Infection of the bone.
Usually bacterial.
Bone tries to contain the core of the infection by forming reactive bone.
Sinus formation can occur (usually to skin or cavity etc).
Difficult to treat; usually surgery or amputation.

142
Q

Means by which infection can be introduced to bone (osteomyelitis)

A

Directly via inoculation/trauma
From adjacent joint
Haematogenously

143
Q

Bone tumors

- benign or malignant?

A

Rare.
Can be benign (expand locally) or malignant (metastasize);
Occur in children and young adults;
Each bone has a preferred site (eg epiphysis);
Eg. Osteo sarcoma

144
Q

Osteosarcoma

A

Most common primary bone malignancy
Occurs in children/adolescents;
Common in metaphysis of long bones (femur near knee);
Typically metastatic at presentation (eg, lungs);
Treated with chemo, surgery;
60-70% survive 5 years post-treatment;

145
Q

Joints (generally)

A

Connection bt 2+ bones that allows for movement and provides structure/support

146
Q

Two types of joints

A

Synarthorses - allow little to no movement

Synovial - allow movement

147
Q

Synovial joints

A

Bones covered with cartilage;
Non-bony surfaces covered with synovial cells (produce fluid);
Surrounded by capsule made up of tendons;
May have meniscus;

148
Q

Meniscus

A

Fibrocartilage disc that absorbs shock.

May be present in synovial joints.

149
Q

Synovial cells

A

cells that cover non-bony surfaces in synovial joints and produce fluid.

150
Q

Osteoarthritis

  • what is it?
  • what does it affect? What causes it?
  • who is at risk?
A

Degenerative joint disease;
Affects weight-bearing joints;
Due to ‘wear-and-tear’ (high level athletes more at risk);
Incidence increases w increased weight and age;

151
Q

Osteoarthritis:

Characteristics (in the joint)

A
  • Exposed bone (cartilage worn down)
  • Bony sclerosis (eburnation)
  • Cyst formation in bone
  • New nodules of bone (osteophytes) form, project into joint space and adjacent soft tissues
  • Inflammation, swelling
152
Q

Osteoarthritis:

Symptoms (clinical presentation)

A
  • Pain (osteophytes, inflammation, microfractures)
  • Crepitus (cartilage degeneration)
  • Swelling and inflammation
  • Deformation (osteophytes, fibrosis, cartilage loss)
  • Loss of mobility
  • Stiffness (improves with rest)
153
Q

Rheumatoid arthritis

  • What is it?
  • populations
  • What happens
A
  • Systemic autoimmune disease affecting synovial joints
  • Any age group
  • Chronic bilateral inflammation of joints
  • Serologic evidence of autoimmune disorder (Abs)
  • Extra-articular manifestations (eg, splenomegaly, skin nodules)
  • Inflamed synovium
  • Inflam cells and fluid expand joint space
  • Inflammation stimulates growth of vessels and synovium; produces factors than injure cartilage and bone
  • Bone fusion (ankyloses) can occur
154
Q

ankylosis

A

Bone fusion

Can occur in rheumatoid arthritis

155
Q

Symptoms of rheumatoid arthritis

A 
Pain
Joint deformity
Limited mobility
Contractures (scarring in joint preventing movement)
Stiffness (improves with movement)
156
Q

Rheumatoid arthritis vs osteoarthritis

A

Rheumatoid:

  • Ankylosis
  • eroding cartilage
  • stiffness improves with movement

Osteo:

  • No ankylosis
  • eroding cartilage
  • subchondral cysts
  • osteophytes
  • Stiffness improves with rest
157
Q

Gout (2)

A

Disease due to hyperuricemia

Deposition of uric acid crystals in various body sites

158
Q

Hyperuricemia

A

too much uric acid

the etiology of gout

159
Q

How does gout work?

A

Uric acid is insoluble in tissue
Lower temperature encourages crystallization (extremities)
Crystals cause inflammation and pain. They may also puncture inflammatory cells, leading to further inflammation.

160
Q

Acute vs chronic Gout

A

Acute - Lasts days; Pain, swelling, problems with mobility, systemic symptoms.

Chronic - Bone deformities, gouty tophi (tumor-like masses of crystals)

161
Q

Primary vs secondary Gout

A

Primary - Metabolic (increased uric acid production) or renal (decreased uric acid excretion)

Secondary - Malignancy (tumor lysis releasing uric acid), chronic kidney disease

162
Q

Preimplantation stage of embryonic development

A

Fertilization followed by cleavage

Blastocyst forms

163
Q

Zygote

A

A fertilized ovum

164
Q

Cleavage-stage embryo

A

Consists of cells whose developmental potential has not been firmly programmed.
Loss of a cell in the 2-8 cells stages can be compensated for.

165
Q

Morula

A

16 cells; day 4

166
Q

Blastocyst

A

Day 5
Cells arrange to form fluid-filled cavity, with inner cell mass inside.
Polarity.
Fate of embryonic cells has been determined.

167
Q

Inner cell mass made up of …

A

Hypoblast and epiblast (future embryo proper)

168
Q

Germ layer formation

  • occurs when
  • what are the layers
A

EMbryonic stage. After implantation.
Gastrulation to make ectoderm, mesoderm, endoderm.
Major axes of final body are established.

169
Q

anlagen

A

argan primordia

Established in early organogenesis

170
Q

Developmental anomalies impact public health. How so?

A

Infant death, long-term morbidity, ID, and other dysfunctions that limit individual productivity.

171
Q

In which trimester is organogenesis most susceptible to developmental defects? Why?

A

First trimester

This is when most tissue differentiation occurs.

172
Q

Causes of developmental malformations (3)

A
  1. Genetic factors
  2. Exogenous teratogens
  3. Chromosomal abnormalities
173
Q

‘gene not compatible with life’

A

Lack of certain genes or lethal mutations can result in nonviable fetal development, resulting in pregnancy loss.

174
Q

Physical teratogens (2 examples)

A

x-rays, corpuscular radiation

175
Q

Chemical teratogens (3 types)

A

Industrial chemicals, drugs, alcohol

176
Q

Thalidamide

A

Chemical teratogen

Children were born with malformed/shortened limbs

177
Q

Fetal alcohol syndrome

A

A result of alcohol as a chemical teratogen.
Most important set of preventable fetal malformations;
Typical facial features (recessed jaw, thin upper lip);
Impaired development of many internal organs;
Impaired mental development; lower IQ;

178
Q

Microbial teratogens

  • 3 types
  • indirect or direct
A

Viruses, bacteria, protozoa

Indirect effects by physically weakening mother, causing reduced fetal weight, growth retardation, or premature birth.

Direct effects due to transplacental passage or microbes and infection of fetus.

179
Q

TORCH syndrome

A

An example of microbial teratogen-caused syndrome.

Marked by involvement of several organ systems.

180
Q

Congenital rubella syndrome

A

An example of microbial teratogen-caused syndrome;
Now prevented by maternal immunization.
Triad of microcephaly, heart disease, petechiae/purpura, eye anomalies

181
Q

Chromosomal abnormalities

  • simply
  • 2 types
A

clinical condition caused by abnormal chromosome constitution in which there is duplication, loss, or rearrangement of chromosomal material

Can be structural or numerical

182
Q

Chromosomes are made up of

A

RNA, DNA and protein

183
Q

Karyotypes

A

Are used to study chromosomes
Prepared from blood sample or another tissue grown in culture.
Plates are banded, and banding patterns are used along with chromosome numbers for diagnosis.

184
Q

Aneuploidy

A

Any chromosome number that is not an exact multiple of the haploid number (23)
Eg, gain or loss of an entire chromosome

185
Q

Hyperdiploidy

A

2n+

186
Q

Hypodiploidy

A

2n-

187
Q

Monosomy

A

Loss of a single chromosome

188
Q

Trisomy

A

Gain of a single chromosome

189
Q

Trisomy 21

  • The syndrome
  • Its features (6)
A

Down’s Syndrome

  • mental retardation
  • Unique facial features / eye abnoramalities
  • Gaping mouth, large protruding tongue
  • Heart diseases
  • Intestinal defects
  • Hand abnormalities
  • Toe abnormalities
190
Q

Genetic sex determination in humans

A

Established at fertilization
Egg carries X and sperm carries X or Y
Y carries SRY, and determines male sex.

191
Q

Phenotypic sex vs genetic sex

A

phenoytpic - appearance of external genitalia

genetic - presence of X or Y second chromosome

192
Q

Turner’s Syndrome

A

Partial or complete absence of one X chromosome.

  • Short
  • Heart-shaped face
  • Webbing of neck
  • Heart disease
  • Broad chest
  • Cubitus valgus
  • Streak ovaries (unable to nurture oocytes, and they are lost early infancy), hypoplastic uterus, amenorrhea
  • Usually infertile
193
Q

Klinefelter’s Syndrome

A

At least one extra X chromosome in a male karyotype (eg, 47XXY)

  • Most common disorder of sex chromosomes
  • Can have more Xs or more Ys, or be 46 XX males with translocation of SRY onto an X during paternal meiosis
  • Tall, long arms and legs
  • Lack of beard, body hair, pubic hair
  • Gynecomastia (breast development)
  • Female-like hips
  • Testicular atrophy, infertility
194
Q

Examples of numerical chromosomal abnormalities (3)

A

Down’s Syndrome
Klinefelter’s Syndrome
Turner’s Syndrome

195
Q

WAGR Syndrome

A

Caused by 11p12-p14 deletion (a structural chromosomal abnormality);
Results in loss of several important genes including WT1, a tumor suppressor gene;
Wilms’ tumor of kidney + Aniridia + Genital malformations + mental Retardation

196
Q

REciprocal translations

A

Transfer of one segment of one chromosome to another non-homologous chromosome;
No loss or gain of clinically relevant information, therefore, not phenotypic consequences;
Reproductive consequences (only 1/3 gametes are normal)

197
Q

Robertsonian translocation variant of Down’s Syndrome

A

A variant where the individual has 46 chromosomes;
Whole arm of acrocentric chromosome (21 to another).

Balanced form: no DS because modal chromosomal number reduced to 45 (lose on 21)
Unbalanced form: Modal chromosome number remains 46. (translocated 21 arm acts as a 3rd 21)

198
Q

Single gene defect (1)

A

A disorder due to one or a pair of mutant alleles at a single locus

199
Q

Characteristics of autosomal dominant disorders

A

Trait seen in heterozygotes
50% chance of transmission to offspring
Trait seen in every generation

200
Q

Example of autosomal dominant disorder (2)

A

Marfan’s Syndrome

Familial hypercholesterolemia

201
Q

Marfan’s Syndrome

A

Autosomal dominant disorder.

  • Elongated head
  • Eye abnormalities
  • Large blood vessels, aortic aneurysm (dissecting, exsanguination)
  • Floppy mitral valve
  • Vertebral deformity
  • Long fingers
  • Bone and joint involvement
202
Q

Familial Hypercholesterolemia

A

Autosomal dominant.
LDL receptor mutation. Reduces cholesterol removal from blood.
Accelerated heart disease, atherosclerosis, lipid deposits.

203
Q

Characteristics of autosomal recessive disorders (2)

A
  • Visible trait only in homozygotes

- Parents are usually asymptomatic carriers

204
Q

Examples of autosomal recessive disorders (5)

A 
Cystic fibrosis
Anemias
Lipidoses (Tay-Sachs, Niemann-Pick)
Mucopolysaccharidoses
AA disorders (lysosomal storage diseases, PKU)
205
Q

Cystic Fibrosis

A

Most common autosomal recessive fetal disease;
Caused by mutation to a chloride transport channel
Affects pancreas, lungs, sweat glands
Screened for

206
Q

Cystic fibrosis is caused by a mutation in what?

A

A chloride transport channel

207
Q

Tay-Sachs

A

Autosomal recessive lipidosis / lysosomal storage disease.

Increased substrates in vacuoles.

208
Q

Phenylketonuria

A

Autosomal recessive disorder
Phenylalanine can’t be broken down to tyrosine;
Phenylpyruvic acid build up causes mental retardation;
Treated with diet changes (phenylalanine deficient diet);

209
Q

X-linked recessive disorders

A
  • Usually only evident in males
  • Gene transmitted from asymptomatic mother
  • Unaffected brothers aren’t carriers, unaffected sisters may or may not be carriers
  • Affected males do not transmit the gene to their sons, but ALL of their daughters are carriers
210
Q

Examples of X-linked recessive disorders (2)

A
  • Hemophilia A and B
  • Fragile X syndrome
    Muscular dystrophies (Duchennes worse than Becker’s)
    Congenital immunodeficiencies
211
Q

Hemophilia A and B

A

X-linked recessive disorder
Mutation in genes involved in coagulation –> bleeding disorders
A has large effects

212
Q

Fragile X Syndrome

- Cause (3)

A 
X-linked recessive disorder;
CGG repeat - more repeates = more severe
Mental retardation (most common cause of mental retardation in males)
213
Q

Most common cause of mental retardation in males

A

Fragile X Syndrome

214
Q

Most common autosomal recessive fetal disease

A

Cystic fibrosis

215
Q

Multifactorial inheritance

A

The trait or disease is the product of several genes; cannot be explained in terms of Mendelian inheritance;
Exogenous and endogenous factors determine the expression and severity of the disease;
Dose effect;
Person’s with a more severe form of the disease have a larger risk of transmitting it to their offspring;

216
Q

what is a dose effect?

A

Determines the severity of the disease that demonstrated multifactorial inheritance.

217
Q

What are some traits that are passed on by multifactorial inheritance?

A

Height, intelligence, blood pressure, metabolism, development

218
Q

What are some examples of diseases that are passed on by multifactorial inheritance? (2)

A

Anencephaly and Cranioarachischisis (failure of spinal cord to close)
Diabetes Tye 2

219
Q

Diabetes Type 2

  • inheritance
  • higher rates associated with…
A

Multifactorial inheritance;
50% of affects persons have relatives with diabetes;
Higher incidence in populations with high rates of intermarriage;
High concordance in monozygotic twins;
Complex interaction bt genetics and the env;

220
Q

Methods of prenatal diagnosis (4)

A
  • Ultrasonographic exam
  • Chorionic villus biopsy
  • Amniotic fluid analysis (amniocentesis)
  • Maternal blood analysis (not invasive!)
221
Q

Ultrasonographic exams are useful for observing (2)

A

Growth of organs and bones

222
Q

Chorionic villus biopsy

A

Can be done at 10-14 weeks;

Karyotype of placental disease reflects that of the fetus;

223
Q

Amniocentesis

A

Amniotic fluid from inside the membrane around the fetus is collected. It contains cells sluffed off by the fetus.
Centrifuge sample and collect cells;
DNA extraction, chromosome analysis, biochemical analysis,

224
Q

Prematurity is defined as

A

<30 weeks and weight < 2500g

225
Q

What is the normal length of pregnancy?

A

38-42 weeks

226
Q

What is the average birth weight?

A

3500g

227
Q

What constitutes immaturity (referring to fetus)

A

<1500 g
Anatomically and functionally immature (most noticeable in lungs and brain);
Cannot survive without medical assistance;

228
Q

What percentage of pregnancies terminate prematurely?

A

5-10%

229
Q

Causes of prematurity (3 groups)

A

Maternal factors: malnutrition, smoking, substance abuse, infection
Fetal factors: infections, malformations, genetic diseases
Placental factors: placental insufficiency

230
Q

Neonatal Respiratory Distress Syndrome

  • cause
  • characteristics
  • complications
A

Immature pneumocytes type II -> surfactant deficiency

Atelectasis (complete or partial lung collapse), alveolar, endothelial injury of lungs
Hypoxia-hyaline membrane

Complications:

  • cerebral intraventricular hemorrhage
  • Hemorrhagic intestinal necrosis
231
Q

Sudden Infant Death Syndrome

  • prevalence
  • risk factors
A

Sudden unexpected death in infants who are 2 > 9 months
Cause unknown
Maternal risk factors: young, low SES, smokers
Infant/fetal risk factors
Most common cause of death in infants beyond immediate neonatal period.

232
Q

Wilms’ Tumor

- Appearance (3)

A
  • Mostly seen in children
  • Hemorrhagic, solid, necrotic tumor
  • Uninvolved kidney
  • Composed of immature cells resembling fetal tubules, primitive glomeruli or renal blastema
  • Bilateral in 5% of cases
  • Good prognosis with surgery and chemo
233
Q

Causes of Wilms’ Tumor

A

Related to mutation of deletion of two tumor suppressor genes: WT1 and WT2

234
Q

3 types of renal cell carcinoma

A

Clear Cell
Papillary
Chromophobe

235
Q

Renal cell carcinoma generally affects which age range?

A

> 50

236
Q

Most common finding in Renal Cell Carcinoma

A

Hematuria (50%)

237
Q

The typical triad of renal cell carcinoma

A

Hematuria, flank pain, palpable abdominal mass

Found only in 10%

238
Q

Which cancer is called the ‘internist’s tumor’ and why?

A

Renal cell carcinoma;

Has nonspecific symptoms and is usually found accidentally

239
Q

Clinical features of renal cell carcinoma

A

Hematuria
Typical triad (hematuria, flank pain, abdominal mass)
Nonspecific symptoms
Paraneoplastic syndromes: hypercalcemia, erythrocytosis (due to EPO production by tumor)

240
Q

Clear Cell renal cell carcinoma

A

Cells have clear cytoplasm, rich in glycogen and fat;
Small capillaries in between;
Yellow-appearing (due to fat)
Nuclear grade: small/round -> big/irregular nuclei
Worst type of renal cell CA; progresses rapidly

241
Q

Papillary renal cell carcinoma

A

Sporadic - solitary tumor
Hereditary - multiple tumors
Papillae with fibrovascular core, epithelial lining and foamy cells

242
Q

Chromophobe renal cell carcinoma

A

Least common
Multiple losses of chromosomes
Distinct cell borders, ‘reisinoid’ nuclei, perinuclear halo
Very good prognosis

243
Q

Which renal cell carcinoma presents with perinuclear halo upon histologic examination?

A

Chromophobe renal cell carcinoma

244
Q

Urothelium

A

Transitional epithelium;
Renal calices, pelves, ureters, urinary bladder, most of urethra;
Specialized to waterproof and withstand prolongued exposure to urine;

245
Q

Urothelial carcinoma

  • source
  • symptom
  • risk factors
A

Derived from urothelium;
Main symptom is hematuria;
Risk factors: smoking, occupational exposure, analgesic drugs, schistosoma;

246
Q

Carcinoma of urinary bladder

  • how common is it?
  • Source
  • prognosis
A

Most common cancer of urinary tract;
usually urothelial carcinoma (may be squamous or adenocarcinoma too)
Variable prognosis

247
Q

Most common cancer of the urinary tract?

A

Carcinoma of urinary bladder

248
Q

Papillary urothelial carcinoma

A

Delicate papillary fronds with thin, fibrovascular stalks

249
Q

Urothelial carcinoma in situ

- Appearance (2)

A

High grade, flat abnormality within bladder mucosa;
Can exist alone or in association with urothelial carcinoma;
Exfoliates easily (mucosal red graularity);

250
Q

Hormone regulation of spermatogenesis

A

FSH and testosterone work together to stimulate spermatogenesis;
LH stimulates Leydig cells (in testes) to produce androgens, which have negative feedback on hypothalamus;

251
Q

Cryptorchidism

A

Congenital malpositioning of testes outside of their normal scrotal location;
3-4% male newborns have retractile testes due to unclosed inguinal canal;
Cryptorchid = one or both testes not in scrotum;
Infertility can result if both testes are cryptorchid;
Cryptorchid testes have 10x risk of undergoing malignant transformation;

252
Q

Balanitis

A

Inflammation of the glans penis

253
Q

Urethritis

A

Inflammation of urethra

254
Q

Prostatitis

A

Inflammation of prostate

255
Q

Epididymitis

A

Inflammation of epididymis

256
Q

Orchitis

A

Inflammation of testes

257
Q

In young men, localized infections are usually due to _________

A

sexual transmission

258
Q

In older men, most infections are related to ______________

A

Urinary retention secondary to prostatic enlargement

259
Q

Genital Herpes

A

Caused by HSV type 2. Virus invades skin, producing grouped vesicles with clear fluid;
lesions on glans skin of penis or scrotum;
no permanent cure, antiviral drugs provide relief;

260
Q

Gonorrhea

A

Burning on urination

Yellow urethral purulent discharge

261
Q

Nongonococcal urethritis

A

Caused by chlamydia or mycoplasma
Most common STD
No purulent discharge (as in gonococcal infections)

262
Q

Syphilis

  • cause
  • Primary
  • Secondary
  • Tertiary
A

Caused by Treponema pallidum
Primary: CHANCRE and inguinal lymphadenopathy
Secondary:
- systemic spread of spirochettes 2mo -2yrs later
- systemic symptoms: fever, macular rash, condyloma latum, hepatitis, organ inflammation
Tertiary: CNS, CV lesions; ~20yrs later; incurable

263
Q

Chancre

A

Painless, indurated ulcer that heals spontaneously;

Characteristic of the secondary stage of syphilis

264
Q

Tumors of testis

  • How common
  • age group
  • tissue source
  • Prognosis
A
  • rare
  • peak 25-45 yrs
  • Usually malignant but treated with surgery + chemo for 90% survival these days
  • Most are germ cell tumors (some sex cord tumors)
265
Q

Leydig cell tumours

A
  • Produce excessive testosterone, which can cause precocious puberty in preadolescent males
  • 10% malignant
266
Q

Sertoli cell tumor

A
  • usually benign

- Cells arranged into tubules resembling an immature testis.

267
Q

Testicular Lymphoma

A
  • Rare
  • Most common testicular cancer in old men
  • Non-Hodgkin’s lymphoma (large cell)
  • Usually disseminated (rarely confined to testes)
268
Q

Seminoma

A

A germ cell tumor of testis in adults

- Really easy to treat/cure

269
Q

Malignant nonseminomatous germ cell tumor (NSGCT)

3 types

A

Embryonal carcinoma
Teratoma
Yolk sac tumor

270
Q

Embryonal carcinoma

A

Malignant nonseminomatous germ cell tumor (NSGCT);
20-30yrs age group;
More aggressive than seminomas;
Necrotic and hemorrhagic tumor composed of sheets of malignant cells;

271
Q

Teratoma

A

Malignant nonseminomatous germ cell tumor (NSGCT);
Rare in pure form;
Prepubertal - likely benign;
More commonly mixed and malignant (in adults);
Mixture of elements from more than one germ layer;

272
Q

Yolk sac tumor

A

Malignant nonseminomatous germ cell tumor (NSGCT);
Secreted AFP;
Endodermal sinuses- resembling primitive glomeruli;
Usually benign in prepubertal children;

273
Q

Mixed germ cell tumor

A

Portions of seminoma and portions of malignant nonseminomatous germ cell tumor (NSGCT)

Not a good prognosis;

274
Q

Two man pathologies of the prostate

A

Benign prostatic hypertrophy

Carcinoma of the prostate

275
Q

Benign prostatic hypertrophy

A

Reactive enlargement of the periurethral portion of the prostate gland;
Nodular hyperplasia compresses urethra, making urination difficult;
Pathogenesis not fully understood;
Treat with transurethral resection or prostate;

276
Q

Complications of benign prostatic hypertrophy

A
  • hydronephrosis
  • Reflux nephropathy
  • Hydroureter
  • Muscular hypertrophy
  • Urine stasis, bladder dilation, infections
277
Q

carcinoma of the prostate

  • prevalence (2)
  • cause (2)
  • where is it
  • markers
  • metastases
A
  • Most common cancer of internal organs in males
  • African > European > East asian
  • Cause unknown: testosterone plays a role
  • Tumor of old age; longer life span accompanied by greater incidence of this cancer;
  • Most often in peripheral parts of prostate
  • Prostate Specific Antigen (PSA) is a marker (but low specificity)
  • Metastases to local lymph nodes, vertebrae, other bones, internal organs
  • Bone metastases may be osteolytic or osteoblastic
278
Q

Primary carcinoma of penis

  • prevalence
  • risk
  • type
  • development
A
  • Rare in USA, more common in other parts of the world
  • Circumcision may reduce risk
  • Most commonly squamous cell
  • Metastases to inguinal lymph nodes first
  • Prognosis depends on stage
279
Q

Hypofunction of the pituitary can be caused by (3)

A

agenesis (failure of organ to develop) / atrophy / destruction;
Acute postpartum insufficiency;
Tumors that compress the normal pituitary;
Trauma to the base of the skull or intracranial surgery;

280
Q

Hyperfunction of the pituitary can be caused by (2)

A

Tomur

Hyperplasia

281
Q

Acute postpartum pituitary hypofunction is due to:

A

Ischemia related to postpartum pituitary necrosis (may be the result of hypovolemic shock/blood loss)

282
Q

How does panhypopituitarism of adults patients present?

A

General weakness, cold intolerance, poor appetite, weight loss, and hypotension

283
Q

Localized mass of pituitary would cause

A

compression of optic chiasm or basal portion of brain

284
Q

Prolactinoma

A

Pituitary tumor

would cause amenorrhea and galactorrhea

285
Q

Somatic adenoma

A

Causes acromegaly in post pubertal patients;

Causes gigantism in prepubertal patients;

286
Q

Acromegaly

A

A characteristic feature of adult somatic adenoma;

Enlargement of feet, hands, jaw caused by growth-hormone secreting tumours of the pituitary;

287
Q

Example disease of the posterior pituitary (1)

A

Diabetes insipidus

288
Q

Diabetes Insipidus

  • Location of disease
  • Disease characterized by (2)
  • Possible causes
A

Posterior pituitary disease;
Lack of ADH -> polyuria;
Caused by tumors, infections of brain meninges, intracranial hemorrhage, trauma of bones at base of skull or transection of pituitary stalk;

289
Q

Hyperthyroidism: Example disease

A

Graves’ Disease

290
Q

Graves’ Disease

  • prevalence
  • pathology
A

85% of all hyperthyroidism cases
More often seen in women;
Autoantibodies to the TSH receptor on thyroid follicular cells;

291
Q

Exophthalmos (bulging eyes) is characteristic of which disease?

A

Graves’ Disease

292
Q

Clinical features of Graves’ Disease

A
  • Exophthalmos (bulging eyes) and pretibial edema;
  • Thyroid is warm, nodular, diffusely enlarged;
  • Diarrhea, weight loss;
  • Warm/sweaty skin;
  • Restlessness, nervousness, emotional lability;
  • Muscle tremor, tachycardia;
293
Q

Hypothyroidism: Possible Causes

A
  • Developmental disorders: aplasia of thyroid
  • Thyroiditis: Hashimoto’s disease
  • Thyroidectomy
  • Iodine deficiency (most common nutritional cause of hypothyroidism)
294
Q

Hypothyroidism: Clinical features

A

In children: Dwarfism and mental retardation

In adults:

  • Myxedema (doughlike puffy skin)
  • Heart failure (bradycardia)
  • Constipation
  • Cold intolerance
  • Muscle weakness
295
Q

Goiter caused by:

A
  • Caused by iodine deficiency or idiopathic
296
Q

What is a Goiter?

  • what is it?
  • secondary changes (3)
  • Symptoms
A

Nodular goiter consists of nodules that enlarge and deform the thyroid;
Secondary changes include calcification, hemorrhage, and atrophy;
Most are nontoxic;
Symptoms related to compression of larynx;

297
Q

Benign thyroid tumor

A

Follicular adenoma

298
Q

Malignant thyroid tumors: 4 types

A

Papillary carcinoma
Follicular carcinoma
Medullary carcinoma
Anaplastic carcinoma

299
Q

Papillary carcinoma of thyroid

A

90% of malignant thyroid tumors

Low grade; favourable prognosis

300
Q

Medullary carcinoma of the thyroid

A

The cancer is derived from C cell, which produce calcitonin;

301
Q

Anaplastic carcinoma

A

Rare;

Most patients die within 1 year of diagnosis;

302
Q

Hyperparathyroidism: primary vs secondary

A

Primary - Due to parathyroid hyperplasia or neoplasia

Secondary - Chronic renal failure

303
Q

Consequences of hyperparathyroidism

A

Stone Bones Moans and Groans

Parathyroid hormone causes BONE resorption, indirectly stimulating calcium absorption in intestine (hypercalcemia).
Hypercalcemia causes renal STONES, psychiatric manifestations (MOANS), and stomach ulcers (GROANS)

304
Q

Adrenal Hyperfunction: Example disease

A

Cushing’s Syndrome

305
Q

Cushing’s Syndrome

A

= Hypercortisolism

  • Moon face / puffy
  • Obesity, cuteneous striae
  • Emotional instability
  • Buffalo hump
  • Osteoporosis
  • Muscle wasting
306
Q

An example of acute adrenal hypofunction/insufficiency

A

Water-house friedrichsen syndrome in meningococcal sepsis

307
Q

Chronic adrenal insufficiency/hypofunction maybe the result of (4)

A
  • Autoimmune diseases (most common)
  • Tumors
  • Tuberculosis
  • Amyloidosis
308
Q

How does Addison’s Disease present?

A

Fatigue, wight loss, nausea, hypotension, frequent syncope, susceptible to recurrent infections.

Adrenal hypofunction

309
Q

Example of a nonfunctioning adrenal tumor?

A

Adrenocortical adenoma

310
Q

A malifnant tumor of adrenal medulla in children

A

Neuroblastoma

311
Q

Pheochromoblastoma

A

Usually benign tumor of adrenal medulla in adults;
VMA in urine important for diagnosis;
Usually benign, solitary tumors tat secrete Epi and NE;
Patients have: malignant hypertension, heart palpitation, sudden dizziness/blurred vision, headaches, increased catecholamines in urine;

312
Q

Liver hilum

A

Three main structures enter the liver at the hilum:

Portal vein and hepatic artery and common bile duct

313
Q

What does the inferior vena cava do in regards to the liver?

A

Drains blood away from the liver

314
Q

Portal tract/triad

A

Hepatic artery + portal vein + bile duct

315
Q

Hepatocytes

A

workhorses of liver; storage; metabolism

316
Q

Functions of the liver

A

Excretion (bile)
Metabolic (metabolism of fats, carbohydrates, proteins, drugs)
Storage (carbohydrates, fat, vitamins)
Synthesis (proteins like albumin)

317
Q

Clinical signs of chronic liver disease (JAKE’S V)

A

Jaundice
Ascites (fluid accumulation in abdominal cavity)
Kidney and lung symptoms
Encephalopathy (mental difficulties due to excess NH4)
Splenomegaly
Varices (expanded blood vessels at risk of bleeding)

318
Q

Hepatitis A Virus

A

ssRNA;
Fecal-oral spread (contaminated food/water);
Illness may arise 15-45 days after exposure;
Brief illness (days);
Acute hepatitis (inflammation, some hepatocyte apoptosis and necrosis);
Vaccine available;

319
Q

Hepatitis B Virus

A

dsDNA;
‘ground glass’ inclusions of HBV seen in hepatocytes;
Parenteral, vertical, or sexual transmission;
40-180 days incubation period;
Can cause acute or chronic liver disease;
High risk of chronic liver disease if acquired at birth/as child;
Vaccine available;

320
Q

Hepatitis C Virus

A 
ssRNA; 
Portal-based inflammation, including lymphoid aggregate; 
Sexual and parenteral transmission; 
May be asymptomatic for many years;
Major cause of chronic liver disease; 
No vaccine, but pricy treatments;
321
Q

Hepatitis D Virus

A

INCOMPLETE ssRNA virus;
Needs Hep B to replicate;
May be infected with B and D at the same time (more aggressive, chronic disease);
May be infected with D after B (superinfection; may cause acute liver failure);

322
Q

Hepatitis E Virus

A

ssRNA;
Fecal-oral and zoonotic transmission;
Typically causes mild-severe hepatitis, like HAV;
May cause chronic liver disease in certain populations (immunosuppressed);

323
Q

Fatty Liver Disease

A

Alcoholic or non alcoholic;
Liver contains >5% fat (Steatosis);

Progression to STEATOHEPATITIS: Fat injures cell organelles and membranes. Eventual necrosis and collapse of the cytoskeleton;
Necrosis and resulting inflammation induce fibrosis;

324
Q

Risk factors for non-alcoholic Fatty Liver Disease

A

Obesity
Diabetes
Metabolic syndromes
Certain drugs

325
Q

Steatosis

A

= Fatty liver disease

Defined as liver containing >5% fat

326
Q

Steatohepatitis

A

Fatty Liver Disease.

The next step after steatosis that marks fat injuring cells of liver.

327
Q

Autoimmune Hepatitis

- Presentation

A

Plasma cells injure hepatocytes;
Commonly young females;
Most patients have other autoimmune disorders;
Presentation ranges from asymptomatic to acute liver failure;

328
Q

Primary Biliary Cholangitis

A

Autoimmune disease;
Typically middle-aged females;
Immune-mediated destruction of small bile ducts;
Florid duct lesions - granulomatous inflammation (destroys small bile ducts);
URSO treatment (bile acid mimic);

329
Q

Florid duct lesions

A

Granulomotous inflammation that destroys small bile ducts in Primary Biliary Cholangitis;

330
Q

Primary Sclerosing Cholangitis

A

Unknown etiology, possibly autoimmune;
Usually young adult males;
Associated with ulcerative colitis;
Fibro-obliterative destruction of large bile ducts;
Periductal, ‘onion-skin’ fibrosis surrounds and detroys bile ducts, followed by a scar;

331
Q

Alpha-one-anti-trypsin deficiency

A

Autosomal recessive disorder
In liver, accumulation of A1AT protein leads to hepatocyte injury;
In lungs, absence of A1AT enzyme allows elastase to proceed uninhibited, resulting in destruction of lung parenchyma (emphysema);

332
Q

Hereditary Hemochromatosis

A

Autosomal recessive;
HFE gene;
Liver normally produces HEPCIDIN, which binds to transglutaminase in small intestinal cells and regulate iron absorption;
In HH, hepcidin production is altered, so intestine absorbs too much iron.
Iron deposited in hepatocytes, and other sites causing injury;

333
Q

Iron stain of liver shows iron as ______.

A

blue

334
Q

Wilson’s Disease

A

Autosomal recessive
ATP7B gene;
Low or secreased ceruloplasmin leads to accumulation of copper in tissues, which leads to damage;

335
Q

Copper stain shows copper as ____

A

red

336
Q

Cirrhosis

A

All modes of liver injury can cause cirrhosis;
Hepatocytes and/or bile duct injury (cell necrosis, inflammation, fibrosis, vascular injury and compromise);
Injury leads to regeneration of liver cells in NODULES surrounded by fibrosis;

337
Q

Cirrhosis leads to

A
  • Increased risk of death
  • Possible liver transplantation
  • Increased risk of cancer: hepatocellular carcinoma (from hepatocytes), or cholangiocarcinoma (arising from bile ducts)
338
Q

Where is the head of the pancreas located?

A

In the steep curve of the duodenum

339
Q

Functions of the pancreas

A

Exocrine: Secretes digestive enzymes into duodenum;

  • Amylase, lipidase, peptidase
  • From acini and ducts

Endocrine: Secretes hormones into circulation ot act on distant body sites;

  • insulin and glucagon for blood sugar reglulation;
  • From endocrine islets;
340
Q

Symptoms of diabetes

A

Poluria
Polydyspia (excess thirst)
Polyphagia (excess hunger)
Organ damage (retinopathy, neuropathy, vascular disease)

341
Q

Type 1 diabetes

A 
Sudden onset in childhood
Patients typically not obese
Autoimmune; Abs target insulin-producing pancreatic cells;
Absolute insulin deficiency; 
patients require insulin therapy;
342
Q

Type 2 diabetes;

A

Patients are typically middle-aged, frequently obese and many have other metabolic syndrome components;
Gradual onset;
Insulin RECEPTORS on target tissues become resistant to insulin;
Treatment includes lifestyle changes, oral medication, insulin;

343
Q

Acute Pancreatitis

  • what is it?
  • pathology
  • common causes (2)
A

Acute inflammation of the pancreas;
Exocrine pancreatic cell death - release digestive enzymes, damaging remaining pancreas and adjacent fat (autodigestion);
Commonly caused by alcohol or bile stones that clog the duct, causing everything to back up;

344
Q

Possible effects of acute pancreatitis (4)

A

altered homeostasis in the blood (Ca regulation);
Inflammatory/necrotic reaction;
Spread of inflammation to liver walls or abdomen;
Formation of pseudocyst;
Diabetes (destroyed islets);

345
Q

Chronic Pancreatitis

A

Fibrosis and mild inflammation of pancreas
Gradual onset
May be preceded by acute pancerastitis
Alcohol is etiology in 70%

346
Q

Results of chronic pancreatitis

A

endocrine insufficiency (diabetes)
Exocrine insufficiency (malabsorption)
pain (fibrosis entraps nerves)
increased risk of pancreatic cancer

347
Q

Pancreatic ductal adenocarcinoma

A 
Most common pancreatic cancer
usually middle-aged to elderly patients
Most occur in head of pancreas
Jaundice is common presenting symptom
80% of patients have cancer outside of their pancreas at time of diagnosis (bad bad boy)
348
Q

neutropenia can be caused by (2)

A

bacterial infections

drugs (eg, closapine)

349
Q

Nephroblastoma

A

malignant tumor of the adrenal medulla in children

Path3000 (2 decks)

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