Usmle Fa Basic Pathology

Front 1

Hyperplasia

Back 1

Cells have increased in number—hyperplasia

Front 2

Dysplasia

Back 2

Abnormal proliferation of cells with loss of size, shape, and
orientation

Front 3

In Situ Carcinoma

Back 3

* Neoplastic cells have not invaded basement membrane
• High nuclear/cytoplasmic ratio and clumped chromatin
• Neoplastic cells encompass entire thickness
• Tumor cells are monoclonal

Front 4

Invasive carcinoma

Back 4

* Cells have invaded basement membrane using collagenases and hydrolases
• Can metastasize if they reach a blood or lymphatic vessel

Front 5

Metastases

Back 5

Spread to distant organs
• Must survive immune attack
• “Seed and soil” theory of metastasis
• Seed = tumor embolus
• Soil = target organ—liver, lungs, bone, brain . . .
• Angiogenesis allows for tumor survival
• decreased cadherin, increased laminin, integrin receptors

Front 6

Metaplasia

Back 6

1 adult cell type is replaced by another. Often 2° to irritation and/or environmental exposure (e.g., squamous metaplasia in trachea and bronchi of smokers)

Front 7

Dysplasia

Back 7

Abnormal growth with loss of cellular orientation, shape, and size in comparison to normal tissue maturation; commonly preneoplastic

Front 8

Name reversible cellular - plasias

Back 8

Hyperplasia, metaplasia and dysplasia

Front 9

Anaplasia

Back 9

Irreversible change. Abnormal cells lacking differentiation; like primitive cells of same tissue, often equated with undifferentiated malignant neoplasms. Little or no resemblance to tissue
of origin.

Front 10

Neoplasia

Back 10

A clonal proliferation of cells that is uncontrolled and excessive

Front 11

Desmoplasia

Back 11

Fibrous tissue formation in response to neoplasm.

Front 12

Grade

Back 12

Degree of cellular differentiation based on histologic appearance of tumor
(The character of the tumor)

Front 13

Stage

Back 13

Degree of localization/spread based on site and size of 1° lesion, spread to regional lymph nodes

Front 14

Tumor staging system (TNM)

Back 14

T = size of Tumor
N = number of involved lymph nodes
M = metastases

Front 15

What are benign and malignant tumors of bone?

Back 15

Rhabdomyoma Rhabdomyosarcoma

Front 16

Name malignancies associated with Down syndrome

Back 16

ALL (we ALL fall Down),
and AML

Front 17

Name malignancies associated with Xeroderma pigmentosum, Albinism

Back 17

Melanoma, basal cell
carcinoma, and especially
squamous cell carcinomas
of skin

Front 18

Name malignancies associated with chronic atrophic gastritis, pernicious anemia, postsurgical gastric remnants

Back 18

Gastric carcinoma

Front 19

Name malignancies associated with Tuberous sclerosis

Back 19

Astrocytoma, angiomyoma, lipoma, and cardiac
rhabdomyoma

Front 20

Name malignancies associated with Barrett’s esophagus (chronic GI reflux)

Back 20

Esophageal
adenocarcinoma

Front 21

Paget’s disease of bone associated with

Back 21

2° osteosarcoma and
fibrosarcoma

Front 22

Autoimmune diseases (e.g., Hashimoto’s thyroiditis and myasthenia gravis are associated with

Back 22

Lymphoma

Front 23

Dysplastic nevus is commonly associated with what?

Back 23

Malignant melanoma

Front 24

Radiation exposure is associated with what types of malignancies

Back 24

Sarcoma, papillary thyroid
cancer

Front 25

What are oncogenes?

Back 25

Gain of function cancer genes. Need damage to only 1 allele to start malignant growth

Front 26

CML is associated with mutation in which gene?

Back 26

abl - mutated Tyrosine Kinase Protein

Front 27

Burkitt's lymphoma is associated with mutation in which gene?

Back 27

c-myc

Front 28

Colon cancer is associated with mutation in which gene?

Back 28

ras

Front 29

Multiple endocrine neoplasia (MEN) types II and III is associated with what type of mutation?

Back 29

tet

Front 30

Rb gene mutation is associated with what malignancies?

Back 30

Retinoblastoma, osteosarcoma

Front 31

BRCA1 and BRCA2 are associated with which malignancies?

Back 31

BRCA1 - Breast and ovarian cancer,
BRCA2 - breast cancer

Front 32

p53 mutation is associated with which malignancies?

Back 32

Most human cancers, Li-Fraumeni syndrome

Front 33

What type of malignancy is colon cancer associated with?

Back 33

DCC—Deleted in
Colon Cancer.

Front 34

What type of malignancy is pancreatic cancer associated with?

Back 34

DPC—Deleted in
Pancreatic Cancer.

Front 35

CEA is a tumor marker for which malignancies?

Back 35

Carcinoembryonic antigen. Very nonspecific produced by 70% of colorectal and pacreatic cancers; also produced by gastric and breast
carcinomas

Front 36

alpha-fetoprotein is a tumor marker for which malignancies?

Back 36

Normally made by fetus. Hepatocellular carcinomas.
Nonseminomatous germ cell tumors of the testis
(e.g., yolk sac tumor).

Front 37

h-CGH

Back 37

Hydatidiform moles, Choriocarcinomas, and
Gestational trophoblastic tumors.

Front 38

Alkaline Phosphatase

Back 38

Metastases to bone, obstructive biliary disease, Paget’s disease of bone

Front 39

Bombesin

Back 39

Neuroblastoma, lung and gastric cancer

Front 40

TRAP staining stains what?

Back 40

Tartrate-resistant acid phosphatase. Hairy cell TRAP leukemia—a B-cell neoplasm
(TRAP the HAIRY animal)

Front 41

Describe the mechanism of DIC

Back 41

Disseminated Intravascular Coagulopathy:
1. activation of coagulation sequenc e through trauma -- leads to disseminated thrombi
2. Consumption of coagulation factors and platelets to sub-hemostatic levels
3. Activation of fibronolysis
4. Tissue hypoxia, microinfarcts and hemorrhage

Front 42

Describe Lab Findings in DIC

Back 42

Increased PT and PTT because most clotting factors have been used up

Front 43

Name three diseases where we see shistocytes

Back 43

1. Thrombic Thrombocytopenia Purpura 2. Thrombotic Microangiopathy
3. Disseminated Intravascular Coagulopathy

Front 44

Describe the mechanism of Thrombotic Thrombocytopenia Purpura?

Back 44

The mechanism is the lack of a protease that cleaves vWF back to its normal size (hereditary or adapted through immune response). Ultra large vWF does not clot, but snags many platelets, this leads to thrombocytopenia without overwhelming consumption of clotting factors.

Front 45

Describe the bleeding pattern for TTP?

Back 45

Ptechiae bleeding because we are dealing with platelet disorder (thispattern is characteristic for thrombocytopenia)

Front 46

Name the first line of treatment for DIC?

Back 46

1. threat the underlying cause -frozen blood plasma since most blood clotting factors (including fibinogen).
Also, give heparin in patients with clinical thrmbosis
3. Can also give inhibitor concentrates - antithrombin, protein C

Front 47

What type of necrosis is gangrene?

Back 47

Coagulative necrosis

Front 48

Why would someone in DIC develop a gangrene?

Back 48

Multple disseminated thombotic events take place in DIC. Thrombi lead to localyzed hypoxia and consequenty to necrosis in the areas deprived of oxygen

Front 49

Define Hyperthrophy

Back 49

An increase in the size of an organ or tissue due to an increase in the size of cells.
Eg. increase in skeletal muscle mass as a response to exercise

Front 50

Define Hyperplasia

Back 50

increase in the size of an organ or tissue due to an increase in teh size of cells
Eg. glandular proliferation in breast during pregnancy

Front 51

Define Aplasia

Back 51

Is a failure of cell production/
Ex. agenesis, or absence of an organ due to a failure of production in embryonic development

Front 52

Define Hypoplasia

Back 52

Decrease in cell production that is less extreme than aplasia
Eg. partial lack of growth and maturation of gonadal structures in Turner syndrome

Front 53

Define Atrophy

Back 53

Decrease in the size of an organ/tissue due to a decrease in the mass of preexisting cells. Eg. due to aging, denervation, lack of endocrine stimulation

Front 54

Define Metaplasia

Back 54

Replacement of one differentiated tissue by another.
Eg. Barrett's esophagus

Front 55

What is Barretts' Esophagus?

Back 55

Long standing GERD (gastro-esophageal reflux disease) can cause adenocarcenoma. This leads to a columna metaplasia - change of pseudostratified columnar epithelium with cilia and goblet cells to columnar epthelium normally seen in stomach

Front 56

What are the causes of hypoxic cell injury?

Back 56

Normally results from hypoxia which can result from the following:
1. ischemia (obstrution of arterial blood flow)
2. anemia - reduction in RBC mass
3. CO poisoning
4. Decreased perfusion

Front 57

Name adaptive responses to cell injury

Back 57

Hyperthrophy (increase in size)
Athrophy (decrease in size)
Hyperplasia (increase in cell number)
Metaplasia (change from one differentiated tissue type to another)

Front 58

Define involution

Back 58

Decrease in the number of organ cells when the organ is no longer needed, for example, Thymus

Front 59

Define Necrosis

Back 59

The sum of degradative and inflammatory reactions occuring after tissue death caused by injury (hypoxia, exposure to toxic chemicals).
It occurs within living organisms

Front 60

Define Autolysis

Back 60

Refers to degradative reactions in cells caused by intracellular enzymes idigenous to the cell. Postmortem autolysis occurs after the death of the whole organism and is NOT necrosis

Front 61

Name four types of necrosis

Back 61

1. Coagulative necrosis
2. Liquefactive necrosis
3. Caseous necrosis
4. Fat necrosis

Front 62

Describe Coagulative Necrosis

Back 62

1. Results most often from cutting off a blood supply to an organ (ischemia).
Most prevalent in the heart and the kidney
3. General preservation of tissue architecture
4.Increased cytoplasmic eosinophilia due to protein denaturation and loss of cytoplasmic RNA

Front 63

Describe Liquefactive Necrosis

Back 63

1. Most often caused by bacterial infections or an interraption of a blood supply
2. Frequent in brain and liver
3. Due to enzymatic digestion
4. Tissue no longer looks intact like in coagulative, but is actively digested

Front 64

Describe Coagulative Necrosis

Back 64

Front 65

Describe this type of cellular response to sublethal injury

Back 65

These are hydropic changes in the hepatocypes. We see how some cells look more swollen and pale

Front 66

Describe cell response to sublethal or reversible damage

Back 66

1. Hydropic changes in the kidney
2. Fatty changes in the liver

Front 67

Describe this adaptive response to reversible injury

Back 67

This is a hydropic change in the kidney. Decreased Na+ pump --> hydrophic changes --> cells swell and now look more pale and distended

Front 68

Describe this cellular response to sublethal injury

Back 68

This is fatty liver.
We see an enlargement of individual hepatocytes.
Oily feel of the organ on a gross level.
Yellowish coloration.
Hepatocytes accumulate fate granules (steatosis).
Cessation of alcohol consumption can cause cells to reverse these morphologic changes

Front 69

Describe this cellular respionse tosublethl injury

Back 69

This is fatty liver on a microspic level. We see that hepatocypes accumulated fat.
Again, this is a reversible change

Front 70

Describe Caseous Necrosis

Back 70

1. Shares features of both coagulative and liquefactive necrosis
2. Normally caused by TB (tubercolous granuloma)
3. Architecture is not preserved but tissue is not liquified. Gross appearance is soft and cheese like.
4. Histologic appearance is amorphous
5. Has increased affinity for eosinophilic dyes

Front 71

Define Fat Necrosis

Back 71

Usually happens with liberation of pancretic enzymes with autodiestion of pancretic parenchyma or trauma to fat cells.

Front 72

Understand the mechanisms of cellular responses to injury

Back 72

none

Front 73

Identify the mechanism of necrosis

Back 73

Coagulative necrosis (gross view)

Front 74

Indentify the type of necrosis in this cardiac tissue

Back 74

This is coagulative necrosis. We see that cellular arcitecture is preserved here, but also can observe slow nuclear fragmentation (on the right we see nuclear fragements instead of cell nuclei)

Front 75

Name necrosis type

Back 75

Coagulative (pale or anemic) necrosis. Renal arteries through renal hilum became occluded - resulting in a "pale" or "anemia" infarction
Again, we see no living tissue, yet the architecture is preserved.

Front 76

Name the type of necrosis

Back 76

This is also coagulative necrosis. We see that the light area is dead due to hypoxia. The rest (darker area) is alive because it receives oxygen by diffusion

Front 77

Name the type of necrosis

Back 77

This is again coagulative necrosis due to adrenal infarct

Front 78

Name the type of necrosis

Back 78

Liquefactive necrosis due to a bacterial infection in the liver

Front 79

Name the type of necrosis

Back 79

Liquefactive necrosis in the brain

Front 80

Name necrosis type

Back 80

Liquefactive in the brain - can see stained bacteria in this slide

Front 81

Name necrosis type

Back 81

This is a caseous necrosis. Left: caseous necrosis in the lung due to TB infection. Right: in the lymph node, again due to a TB infection

Front 82

Name necrosis type

Back 82

Caseous in the lung (go from small to large magnification)

Front 83

Name necrosis type

Back 83

Caseous in the lymph node (high magnification) - we can see that architecture is not preserved but the tissue is not liquified. Increased eosinophilic staining

Front 84

Name necrosis type

Back 84

This fat necrosis in mesentery. We can see necrotic fat cells, inflammation

Front 85

Name necrosis type

Back 85

Again, this is a fat necrosis (high mag)

Front 86

Name necrosis type

Back 86

Fat necrosis in the pancreas

Front 87

Name necrosis type

Back 87

Fat necrosis in the pancreas

Front 88

Name necrosis type

Back 88

Fat necrosis in accute pancreatitis

Front 89

Is this a necrosis? Why?

Back 89

This is apoptosis, programmed cell death and not a necrosis.

Front 90

Name this process - necrosis, apoptosis or autolysis?

Back 90

This is autolysis.
Looks a bit like coagulative necrosis but no inflammation. Autolysis happens due to ingeneous enzymes as a cell death after death of the entireorganism or removal from the body.

Front 91

Describe hemoglobin structure

Back 91

Hb is a multisubunit, plasma protein. It has
2 alpha and 2 beta globin chains: alpha2beta2 (adult)
other globin subunit types are found in the fetus and newborns (zeta, epsilon, gamma, etc).
Human body contains 750g of Hb which is replaced every ~120 days
Hb also transports H+ and CO2 in addition to O2

Front 92

Desribe Iron coordination in oxyhemoglobin

Back 92

1. Fe2+ requires an octahedral coordination.
2. 4 ligands to Fe2+ are provided by nitrogens in the heme group.
3. A 5th ligand is provided by nitrogen from Histidine-93 in the globin chain, also known as the proximal His.
A 6th ligand is provided by O2 which is sandwiched between the Fe2+ and nitrogen on Histidine-64 (the distal His) in the globin chain.

Front 93

Define this type of anemia

Back 93

Normocytic, normochromic anemia

Front 94

Define this type of anemia

Back 94

Microcytic hypochromic anemia

Front 95

Define this type of anemia

Back 95

Macrocytic normochromic

Front 96

Describe the process of heme sythesis

Back 96

Synthesis starts in the mitochondria, continues in the cytosol, and finishes in the mitochondria.
ALA-synthase and Ferrochelatase are two rate limiting enzymes in the entire heme synthesis pathway.

Front 97

Name the enzyme that upregulates heme synthesis when necessary (excess Fe present)

Back 97

ALA-synthase (ALAS) is the rate limiting enzyme.

ALAS protein levels are upregulated in response to increased iron (Fe2+) in erythroid cells.

the ALAS mRNA has a “cis-acting” iron response element (IRE) that modulates the rate of translation of the mRNA to protein.

Front 98

At the level of which enzymes is heme synthesis pathway regulated?

Back 98

Feedback inhibition regulates heme synthesis at two levels:
-ALA-synthase
-ferrochelatase

Front 99

Describe pathophysiology of Anemia of Lead Poisoning (Plumbism)

Back 99

Lead exposure from: paint, gasoline fumes, lead pipes in plumbing, contaminated foods.

Pb targets many molecules vital to cell metabolism. Heme synthesis pathway especially sensitive to Pb.

ALA-dehydratase and ferrochelatase most sensitive Pb targets in pathway -- Lead inhibits these enzymes directly as well as alters Iron uptake

Front 100

Describe Clinical Findings in Anemia of Lead Poisoning

Back 100

Presenting symptoms: abdominal pain, motor neuropathy (palsy).
Hematology: often normocytic and normochromic. Microcytic and hypochromic with chronic exposure. Sometimes basophilic stippling due to iron induced aggregates of ribosomes.
Treatment through removal of Pb source and/or chelation therapy with EDTA or dimercapto-succinate

Front 101

What is Congenital ALA-Synthase Deficiency?

Back 101

An ALA-Synthase Deficiency causes anemia. Patients present with Sideroblastic anemia: Erythrocytes are hypochromic and microcytic.

Front 102

What are Porphyrias?

Back 102

Arise from specific inherited defects in enzymes of heme biosynthetic pathway.

Seven distinct porphyrias are described that correlate with deficiencies in each of the seven enzymes.

Front 103

Describe Acute Intermittent Porphyria (AIP)

Back 103

1. Acute Intermittent Porphyria (AIP)
Manifests neurological and psychiatric illness, visceral pain.
Most are due to accumulation of ALA-synthase enzyme.
Treatment with analgesics for pain, maintain morale, alleviate fear. Infusion of hematin (Fe3+ heme).

Front 104

Name this type of anemia

Back 104

Congenital Erythropoietic Porphyria (CEP)
Manifests cutaneous scarring due to photosensitivity.

Accumulated isomers of Uro’gen and Copro’gen result from inhibition of dehydration. These compounds cause oxidative damage when exposed to light.

treatment with spleenectomy or transfusion.

Front 105

Name four different orgains where Hb is produced during development

Back 105

Changes or “switching” in globin chain composition correlate with sites of Hb synthesis during development.
1. Yolk sac
2. Spleen
3. Liver
4. Bone marrow

Front 106

Describe the pathophysiology of Thalassemia

Back 106

Sickle cell disease (HbS) results from mutations in the  chain of Hb that promote self-aggregation of Hb into fibrils.

A Glu to Val amino acid change at position 6 in  chain most common.

Fibril formation precipitates from deoxy form of HbS.

Front 107

Describe two physiologic states of Hemoglobin

Back 107

Hb exists in two general conformations: the T state and R state (Tight and Relaxed).

O2 binds preferentially to the R state:
-OxyHb=R state
-DeoxyHb=T state

O2 binding invokes structural changes in heme:
-Fe2+ is displaced to be in same plane as porphyrin ring.

Front 108

Describe Oxygen binding kinetics of hemoglobin

Back 108

Front 109

Compare Fetal and Adult Hemoglobin

Back 109

Fetal circulation and maternal circulation come in close contact however, oxygen transport relies on exchange of O2, not RBCs.

The pO2 in the placenta is well below that in the maternal circulation (e.g.<20Torr).

Fetal Hb (HbF) must have a higher affinity for O2 than maternal (adult) Hb (HbA) in order to “extract” O2 from the maternal circulation.

Front 110

Describe the effect of 2,3-BPG on Hemoglobin

Back 110

2,3-bisphosphoglycerate (BPG):
Is an allosteric inhibitor of Hb-O2 binding.

Promotes release of O2 from Hb.

Front 111

Provide physiological exoplanation for the higher affinity of Fetal Hb to Oxygen

Back 111

The physiological basis for the ability of the fetus to withdraw O2 from the mothers circulation relies on the property that, in vivo, HbF has a higher affinity for O2 than HbA.
Adult = HbA = alpha2beta2
Fetal = HbF = alpha2gamma2

Front 112

Describe the effect of pH on Hemoglobin

Back 112

H+ is displaced upon O2 binding to Hb. Therefore, increase in H+ drives the reaction backwards.

Lower pH (higher H+ concentration) causes release of O2. This is known as the Bohr effect.

This is a good thing! Working muscles, which demand more O2, propagate acidic conditions e.g. lactic acid.

Front 113

Describe the effect of Temperature on Hemoglobin

Back 113

The heme-O2 binding reaction is exothermic. Therefore, oxygen affinity of Hb drops with elevated temperature.

Again, this is a good thing! Working muscles, which demand more O2, are elevated in temperature.

Front 114

Describe the effect of CO2 on hemoglobin oxygen dissosiation curve

Back 114

CO2, a major product of glycolysis, is generated rapidly in tissues,especially in working muscles.

CO2 reacts with H20 to form carbonic acid.

Dissociated carbonic acid lowers pH and promotes O2 dissociation from Hb via the Bohr effect.

Front 115

How is CO2 transported in the blood?

Back 115

Front 116

What is Carboxyhemoglobinemia?

Back 116

CO (carbonmonoxide) will bind in the heme pocket in place of O2 with about 250 times greater affinity as O2.

Front 117

What is Methemoglobinemia?

Back 117

Elevated levels of methemoglobin in the blood are caused when the mechanisms that defend against oxidative stress within the red blood cell are overwhelmed and the oxygen carrying ferrous ion (Fe2+) of the heme group of the hemoglobin molecule is oxidized to the ferric state (Fe3+).
MetHb is unable to bind and release O2.
Presence of metHb shifts O2 dissociation curve to the left.

Front 118

Describe clinical symptoms of methemoglobinuria

Back 118

Front 119

Describe Glucose metabolism in erythrocytes

Back 119

RBCs are devoid of nucleus, so most of their metabolic funsction is directed at maintenance. Glucose metabolism proceeds through anaerobic glycolysis which yields 2 ATP for each glucose.

Glycolysis occurs in the cytoplasm.

RBC longevity is reliant upon ATP production which is very sensitive to the “fitness” of the enzymes required for glucose catabolism.

Front 120

Name three most critical enzymes in metabolism

Back 120

Glycolysis requires eleven enzymes. Three critical enzymes are:
-hexokinase (HK)
-phosphofructokinase (PFK)
-pyruvate kinase (PK).

Front 121

What is methemoglobin reductase pathway?

Back 121

NADH produced from G3PDH acts as a reducing cofactor for the metHb-reductase enzyme.

This is the major pathway for reducing metHb back to functional Hb.

Non-enzymatic mechanism of metHb reduction require ascorbic acid or methylene blue, which can be applied clinically.

Front 122

Name three most common ROS (reactive oxygen species)

Back 122

O2- is most common in the process of metHb formation from Hb. Also promotes cell lysis via membrane lipid oxidation.

H2O2 is more stable than OH yet both act to oxidize and denature Hb.

Front 123

Describe Hexose monophosphate (HMP) pathway: glutathione reduction

Back 123

Front 124

What is Glucose-6-Phosphate Dehydrogenase Deficiency?

Back 124

The most common RBC metabolic disorder. >2 million people affected.
The G6PD gene is on the X chromosome and demonstrates a recessive X-linked inheritance. i.e. males are most affected.
Deficiencies compromise the RBC defense of oxidation due to the inability to maintain reduced form of GSH.
Two Mutations are most clinically relevant:G6PD A- (in African Americans) and G6PD Mediterranean, both generally decrease the half-life of enzyme.

Front 125

What is Pyruvate Kinase Deficiency?

Back 125

PK deficiency is prevalent in the US, Europe and Japan. ~1% of US population is heterozygous. Overall decrease in ATP compromises repair processes resulting in hemolytic anemia. No effective therapy, treatments include RBC transfusions.


PK deficiency shows autosomal recessive inheritance and is the most common genetic disorder of the glycolytic pathway.

Front 126

Commen on the iron content of a typical diet and how much is usually absorbed/day

Back 126

A typical diet consists of 10-20 mg/day iron, of which ~10% is adsorbed.

A balance is maintained: roughly 1-2 mg iron is lost daily through loss of epithelia.

Under higher demand for iron adsorption increases to 20% of dietary intake.

Front 127

Names two forms in which iron is absorbed

Back 127

Inorganic (Fe2+, Fe3+ salts) or organic (heme). Heme iron is rapidly adsorbed whereas Fe3+ is not very soluble and poorly adsorbed. Fe2+ is more soluble than Fe3+.
Heme is absorbed by machinery completely different to that of inorganic iron. The process is more efficient and is independent of duodenal pH . Consequently meats are excellent nutrient sources of iron.

Front 128

Name three major compartments of iron in the body

Back 128

-Functional
-Transport
-Storage
RBCs contain 70% of body iron. Approx 25% is in storage in ferritin and hemosiderin

Front 129

What is Ferritin?

Back 129

Ferritin is a huge spherical protein (Mw=440,000 Da) consisting of 24 subunits.
It is common to all cells. High levels occur in erythroid precursors.
Forms a “shell” that can encompase >4500 iron atoms.
Iron can reversibly pass through “channels” in the shell.

Front 130

What is Hemosiderin?

Back 130

less-well characterized complex of iron in a ferric hydroxyphosphate form and protein.
It is a storage compartment when ferritin capacity is exceeded.

Front 131

What is Transferrin?

Back 131

Transferrin is a medium-large soluble protein (MW=79,000 Da) that mediates iron transport between tissues.
It is present in plasma and extracellular fluid.
It binds IRON IN 3+ STATE

Front 132

Describe the mechanism of Iron delivery inside the cells

Back 132

1. Uptake into cells is mediate by the transferrin receptor.
2. Apotransferrin has low affinity for the receptor; iron-bound transferrin binds tightly to the receptor.
3. Binding promotes receptor clustering and endocytosis of transferrrin-receptor complexes into an endosome.
4.Acidification of endosome causes iron dissociation (but not transferrin dissociation from the receptor!).
5. Transferrin is recycled and

Front 133

Describe lab values that measure iron status

Back 133

Iron status is determined by laboratory methods that measure ferritin and transferrin-associated iron levels in serum.

Serum iron is characterized by the total iron binding capacity (TIBC) and unsaturated iron binding capacity (UIBC).

Front 134

Define Thrombus

Back 134

Solidified blood
Inside the vascular space
Of a living organism

Front 135

Where intravascular thrombi are usually located?

Back 135

Intravascular, by definition:
Arteries
Veins
Heart chambers
Heart valves

Front 136

Name this

Back 136

Aortic valve thrombus

Front 137

Name potential fates of thrombi

Back 137

Resolve (heal without a trace)
Propagate
Embolize
Organize
Recanalize
Calcify (phlebolith)

Front 138

Name this stage of thrombus formation

Back 138

Recanalization

Front 139

Name three types of emboli

Back 139

Gas: air, nitrogen (the “bends”)
Liquid: amniotic fluid, contrast material, fat after soft tissue trauma or fracture, injectables
Solid: Thrombus is most common; also foreign bodies (bullet, catheter tip), atheroembolism, bone marrow
Thromboemboli can be infected (septic)

Front 140

What are common origins/sites of thromboembolism?

Back 140

Venous (systemic veins to pulmonary arteries)
Arterial (heart or aorta to systemic circulation
Paradoxic (systemic vein, through a septal defect in the heart, to the systemic circulation)

Front 141

Describe this type of embolus

Back 141

This is a saddle embolism

Front 142

Name this type of embolus

Back 142

Fat embolus

Front 143

Name this type of embolus

Back 143

Paradoxic embolus in foramen ovale

Front 144

Define infarct

Back 144

Localized area of ischemic necrosis
Usually caused by vascular blockage
Note: Takes time (4-6 hours) to be seen microscopically

Front 145

Define Infarction

Back 145

The process of production of an infarct

Front 146

Describe two common morphologies of infarct

Back 146

Varies with different tissues and durations:
1. Pale, roughly wedge-shaped in solid organs with single blood supply (e.g., kidneys and spleen)
2. Hemorrhagic, in soft organs with a dual blood supply (e.g., lungs, bowel)

Front 147

What kind of infarct is this?

Back 147

Ischemic splenic infarct

Front 148

What kind of infarct is this?

Back 148

Hemorrhagic infarct of bowel

Front 149

Define ischemia

Back 149

Decreased blood flow to an organ or tissue
Often distinguished from infarction clinically.