Blood, immunity, and GI Flashcards
The liver synthesizes three anti-coagulants what are they?
Antithrombin III
Protein C and S
What would be a good “clot buster” for human use, and what would some bad ones?
TPA good
citrate, EDTA, and oxalate bad (bind free Ca 2+, necessary for life)
Hypercoagulation/platelet disorders
Fat guy smoking and eating a burger
Smoking, DM, low platelets, and atherosclerosis
Impaired hemostasis: Hyper-bleeding states: Impaired platelet function, coagulation defects, and DIC
IPF: purpura, spleen sequestration, decreased production (BM), or increased destruction
CD: Classic hemophilia lack factor VIII, low vit K. Bruising, joint swelling
DIC: caused by infection, sepsis or snake venom. Widespread hemorrhage.
Serum is different from plasma in what important way?
It has no fibrinogen
What are the major plasma proteins and where do they originate?
Albumin: #1 Liver
Immunoglobulin: B-cells
Clotting factors: mainly fibrinogen
What are the agranulocyte cell types?
Monocytes, Macrophages, Lymphocytes (B/T cells), and NK cells.
How long do platelets survive in the body? Where are they destroyed? In what way are they similar to RBC? Where do they come from?
Platelets survive in the body 10 days and are then destroyed by the spleen. They are similar to RBC in that they lack a nucleus, and they come from megakaryocytes.
What do you call a condition of too many or too few erythrocytes?
Polycythemia or anemia
RBC are broken up into what components in the spleen?
Globulin: AA
Heme: Bilirubin
Heme: Fe 2+
What is the difference between conjugated and unconjugated bilirubin?
Uncojugated bilirubin is lipid soluble and toxic to the body, conjugated bilirubin is paired with glucuronic acid via glucuronyl transferase in the liver and made water soluble.
What causes jaundice? Why is it a problem?
Excess unconjugated bilirubin to high volume of RBC destruction, maybe from some anemic condition (hemolytic anemia) Or, decreased excretion from the liver due to cirrhosis or hepatitis.
Very toxic to brain cells (bilirubin)
How do you determine the type and cause of the jaundice?
POO and PEE!
Both dark=hemolytic anemia
Both light= Intrahepatic obstructive jaundice: damaged hematocytes
Light feces, dark urine: Extrahepatic obstructive jaundice, obstruction of bile duct.
What are some clinical manifestations of polycythemia?
Ruddy cyanosis of the face, splenomegaly, hyperplastic BM
How do you treat polycythemia?
Relative: rehydration
Absolute primary: decrease blood volume or viscosity; secondary: treat disorder, like COPD by not smoking.
Anemia is classified by RBC size and hemoglobin content. How is this described?
Normocytic and normochromic
What types of normocytic and normochromic anemia is there?
Posthemmoragic
Aplastic
Hemolytic
Anemia of Chronic disease
Number of RBC had decreased
Genetic hemolytic anemia; not normocytic
Sickle cell, thalassemia, microcytic-hypochromic.
How do you identify Thalassemias?
Overstimulated BM leads to thin and easily broken bone. Bones of the face are wider. Autosomal recessive like sickle cell, problem with the alpha or beta chain of hemoglobin.
What is hemosiderosis?
Storage of excess iron in tissues
What’s the most common anemia worldwide?
Iron deficiency anemia, common for women and young children
What causes pernicious anemia?
Low B12 low intrinsic factor, typically GI problems and not nutritional deficiency.
Leukocyte abnormalities can be non-malignant or malignant. Name some in each category.
Non-malignant: Infectious mononeucleosis and lymphadenopathy (typically an infection)
Malignant: Leukemia (bleeding/infections), multiple myeloma, and malignant lymphoma
Whats the deal with multiple myeloma?
Plasma cell issues, high IgG causing kidney damage
How are lymphomas identified, and what are they?
Large swollen lymph nodes or secondary lymphoid tissue. They are malignancies of lymphoid tissue but may spread to non-lymphoid tissue.
Whats the difference between Hodgkins and Non-Hogkins lymphoma?
Hodgkins: Reed sternburg cells, transformed lymphocytes (multiple nuclei). 75% survival rate
Non-Hodgkins: No reed sternburg cells, decreased B-cells and macrophages. 30% survival rate.
What is hemostasis?
The formation and removal of a blood clot.
Platelet adherence occurs due to two main events; what are they? How do these events facilitate adherence?
Damage or inflammation via: cytokines, LPS, histamine, and serotonin.
These events trigger the endothelium to release Von Wildebrand factor vWF.
How are platelets normally kept in a non-activated state, and what happens to them when they become activated?
Healthy endothelium secretes various molecules to keep platelets in a non activated state, such as PGI2.
Activation of platelets causes degranulation which lead to more activation (pos loop), these granules can promote vasoconstriction, and release growth factors that help repair the endothelium. Also, fibrinogen receptors are exposed.
How is fibrin useful in clotting?
Platelet fibrinogen receptors bind fibrinogen which is converted to fibrin via thrombin. This fibrin then help platelets form a mesh like network.
Is the extrinsic or intrinsic system more important for clotting?
Extrinsic.
How does clot reduction take place?
F-actin works with myosin to cause platelet size to decrease, the clot size is thus reduced and becomes more dense pulling the wound together.
Which vitamin is essential for blood clotting?
K
What are the three major mechanisms of diarrhea?
Osmotic- inability to digest lactose
Secretory- cholera (bacterial toxins increase Cl- secretion)
Motility- post surgical
How can GERD lead to dysphagia?
GERD essentially causes acid reflux that can inflame the esophagus leading to reflux esophagitis. An inflamed esophagus will swell and narrow leading to dysphagia.
What is ulcerative colitis?
It’s an inflammatory bowl disease characterized by ulcerations of the colonic mucosa, specifically the sigmoid colon and rectum.
What are the symptoms and treatment strategy for ulcerative colitis?
Symptoms: frequent diarrhea, melena, and cramping
Treatment: Antibiotics, immunosuppressants, surgery, and I would add fluid and electrolyte replacement also.
What are three major types of malabsorption/malnutrition deficiencies? Briefly describe them.
Pancreatic insufficiency: Enzyme deficiency leads to both pancreatic problems, and fat maldigestion.
Bile Salt deficiency: Liver disease and bile obstruction lead to low cholesterol low bile salts and decreased fat absorption.Also, the loss of fat soluble vitamins.
Lactose deficiency: Inability to break down lactose results in bacterial fermentation that causes; gas, cramping, and osmotic diarrhea.
What are the fat soluble vitamins and what does insufficiency result in?
Vitamin A: night blindness
Vitamin K: easy bruising/purpura
Vitamin E: slow growth and muscle weakness
Vitamin D: decrease Ca2+ absorption and osteoporosis.
What is cirrhosis?
Irreversible inflammatory disease that disrupts function and structure: fibrosis, portal hypertension etc.
What care some of the consequences of portal hypertension? What are the three categories that describe the location of the vascular resistance?
Blood can be shunted away from the liver and hypoxic necrosis develops.
Prohepatic: narrowing of vessels preceding the liver from the heart: stomach, intestines, and spleen.
Intrahepatic: cirrhosis (most common)
Posthepatic: cardiac impairment.
What are four consequences of portal hypertension?
Splenomegaly, Ascities, varicies (extended veins) , and hepatic encephalopathy.
What are some of the dangers of hepatic encephalopathy?
Liver can’t filter toxins effectively and they can reach the brain and cause impairment, such as a flapping tremor.
What’s the best treatment for NAFLD? What type of progression is there?
Insulin sensitivity improvement.
Gradation: steatosis, steatohepatitis, add on fibrosis, then cirrhosis and cancer.
What happens to pancreatic enzymes as a result of pancreatitis?
The enzymes auto-digest pancreatic tissue and get into the blood and damage endothelium, they also increase vascular permeability as detected by a serum amylase test.
Gallbladder issues: under what conditions do gall stones form?
High cholesterol, high bilirubin, low bile salts or reduced clearance. Low fat dieting
What are the two types of peptic ulcers?
Duodenal and Gastric
How do you distinguish between the two types of peptic ulcers?
Duodenal ulcers developmental factors include: H.pylori, increased acid secretion, NSAIDS, and acid secretion brought on by smoking.
Gastric ulcers. H-pylori, normal acid secretion
Stress ulcers are of what type? what causes them?
Ischemic: trauma
Cushing: burn
What does LPS do in the body and what is the connection with obesity?
LPS induces fat gain, fat storage, and IR.
High fat and high carb meals led to increased blood level of LPS especially among the obese who have “leaky” absorption of LPS.
what is an obesogen and can you name some?
Compound that increases weight gain: pesticides, MSG, plastics, and sugary drinks (diet soda related to T2DM 70% greater risk), fructose.
What’s the deal with fructose?
Fructose is associated with increase in Visceral fat gain, increase LPS absorption, increased hepatic ceramide.
Name three types of bariatric surgery. Which one improves insulin sensitivity?
Vertical band, laparoscopic, and gastric bypass. The gastric bypass improves insulin sensitivity.
Why does calorie restriction not work in dieting? What are two simple rule with dieting?
CR leads to decreases in lean mass and consequently resting metabolic rate, reduces bone mass.
Eat less carbs and sugar.
