Patho exam 2 study guide review notes, Study Guides, Projects, Research of Pathophysiology

Patho exam 2 study guide review notes

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ENDOCRINE:
Parathyroid glands
oWhat two things plasma calcium in the parathyroid?
PTH and Vit D
o
What plasma calcium in the parathyroid?
Calcitonin
oHypoparathyroidism vs. hyperparathyroidism
What happens in Hyperparathyroid? What is
elevated? There is TOO MUCH calcium
Ca,
PTH
Clinical symptoms of hyperparathyroidism?
Sx: fragile bones/bone fractures (bones become depleted of Ca),
constipation (GI slows down), kidney stones (abd pain, increased
Ca in blood). Hyperparathyroid is the most common cause of
ASYMPTOMATIC hypercalcemia
Hypoparathyroidism?
Calcium PTH
Clinical manifestations of hypothyroidism
decreased energy metabolism, constipation, bradycardia, lethargy,
confusion, syncope, decreases libido, anemia, lower CO, dyspnea,
reduced production of erythropoietin, dry skin, dry hair, reduced
growth of nails/hair.
Produce parathyroid hormone (PTH), which is the single most important factor in the
regulation of serum calcium concentration. The overall effect of PTH secretion is to
increase serum calcium concentration and decrease the concentration of serum phosphate.
What is the Parathyroid hormones' (PTH) main purpose?
Regulation of serum calcium concentration**.**
The overall effect of PTH secretion is to increase calcium and decrease phosphate.
TSH and secretion of thyroid hormone
ois a condition that results from any cause of increased amounts of thyroid
hormone (TH) levels. Hyperthyroidism is a form of thyrotoxicosis in which
excess amounts of TH are secreted from the thyroid gland.
othe terms thyrotoxicosis and hyperthyroidism are often used interchangeably.
Enlarged goiter, bruit over thyroid, hypercalcemia, decreased PTH, ED, Wt loss,
freq stools, sweating warm skin, hair-fine, soft, elevated upper eyelid, fine
tremor of lid, inc. C/O tachycardia, restless, short attention span.
Hashimoto's vs Graves disease - thyroid
Hashimoto’s (autoimmune) - MOST COMMON form of HYPOthyroidism
oWhat lab would you run to make sure it's Hashimoto's instead of other cause
of hypothyroidism?
Run an ANTI-TPO test. Hashimoto's is Positive for Anti TPO (Anti-thyroid
antibodies): Anti TPO - antibodies attack thyroid gland and destroying it so it is
underproducing thyroxine
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ENDOCRINE:

Parathyroid glands o What two things ⬆ plasma calcium in the parathyroid? PTH and Vit D o What ⬇ plasma calcium in the parathyroid? Calcitonin o Hypoparathyroidism vs. hyperparathyroidism ▪ What happens in Hyperparathyroid? What is elevated? There is TOO MUCH calcium ⬆ Ca, ⬆ PTH ▪ Clinical symptoms of hyperparathyroidism? Sx: fragile bones/bone fractures (bones become depleted of Ca), constipation (GI slows down), kidney stones (abd pain, increased Ca in blood). Hyperparathyroid is the most common cause of ASYMPTOMATIC hypercalcemia ▪ Hypoparathyroidism? ⬇ Calcium ⬇ PTH ▪ Clinical manifestations of hypothyroidism decreased energy metabolism, constipation, bradycardia, lethargy, confusion, syncope, decreases libido, anemia, lower CO, dyspnea, reduced production of erythropoietin, dry skin, dry hair, reduced growth of nails/hair.

  • Produce parathyroid hormone (PTH), which is the single most important factor in the regulation of serum calcium concentration. The overall effect of PTH secretion is to increase serum calcium concentration and decrease the concentration of serum phosphate.
  • What is the Parathyroid hormones' (PTH) main purpose? Regulation of serum calcium concentration. The overall effect of PTH secretion is to increase calcium and decrease phosphate.
  • TSH and secretion of thyroid hormone o is a condition that results from any cause of increased amounts of thyroid hormone (TH) levels. Hyperthyroidism is a form of thyrotoxicosis in which excess amounts of TH are secreted from the thyroid gland. o the terms thyrotoxicosis and hyperthyroidism are often used interchangeably. Enlarged goiter, bruit over thyroid, hypercalcemia, decreased PTH, ED, Wt loss, freq stools, sweating warm skin, hair-fine, soft, elevated upper eyelid, fine tremor of lid, inc. C/O tachycardia, restless, short attention span.
  • Hashimoto's vs Graves disease - thyroid H ashimoto’s (autoimmune) - MOST COMMON form of HYPOthyroidism o What lab would you run to make sure it's Hashimoto's instead of other cause of hypothyroidism? Run an ANTI-TPO test. Hashimoto's is Positive for Anti TPO (Anti-thyroid antibodies): Anti TPO - antibodies attack thyroid gland and destroying it so it is underproducing thyroxine

o How are the labs for HYPOthyroidism? TSH? T3/T4? TSH is high, T3/T4 are low o What are the clinical manifestations of hypothyroidism? decreased energy metabolism, constipation, bradycardia, lethargy, confusion, syncope, decreases libido, anemia, lower CO, dyspnea, reduced production of erythropoietin, dry skin, dry hair, reduced growth of nails/hair. Sx thinning hair, constipation, cold extremities, wt. gain o Graves Disease ▪ Is GRAVES Disease Autoimmune of hyperthyroidism or hypothyroidism? Hyperthyroidism ▪ How do you differentiate between Grave's and Goiter ? Graves is POSITIVE for TSI ▪ Goiter picture ▪ Graves picture + for TSI ▪ How are the labs for Hyperthyroidism? TSH? T3 and T4? TSH is low; T3 and T4 are high ▪ How are the labs for GOITER and Graves? ▪ Same as Hyperthyroidism, except Graves is POSITIVE for TSI ▪ What is TSI? TSI is Thyroid stimulating immunoglobulins Autoimmune disease and results from a form of type II hypersensitivity in which there is infiltration of lymphocytes and stimulation of the thyroid by autoantibodies directed against the TSH receptor. These autoantibodies, called thyroid-stimulating immunoglobulins (TSIs; also called thyroid-stimulating antibodies [TSAbs] or thyroid receptor antibodies [TRAbs]), override normal negative feedback mechanisms. Hypothyroidism – autoimmune, Hashimoto’s disease, iatrogenic loss of thyroid tissue after surgical /radioactive tx for hyperthyroidism, neck radiation therapy, medications, endemic iodine deficiency loss of functional thyroid tissue, lead to a decreased production of TH decreased energy metabolism, constipation, bradycardia, lethargy, confusion, syncope, decreases libido, anemia, lower CO, dyspnea, reduced production of erythropoietin, dry skin, dry hair, reduced growth of nails/hair.

  • Graves’ disease is classified as an autoimmune disease and results from a form of type II hypersensitivity in which there is infiltration of lymphocytes and stimulation of the thyroid by autoantibodies directed against the TSH receptor. These autoantibodies, called thyroid-stimulating immunoglobulins (TSIs; also called thyroid-stimulating antibodies [TSAbs] or thyroid receptor antibodies [TRAbs]), override normal negative feedback mechanisms.
  • SIADH - What happens? explain the labs and clinical manifestations? Do you gain weight? Too much ADH means too much water is being retained
  1. How do you diagnose? Hba1c, fasting plasma glucose, two hour plasma glucose during oral glucose tolerance testing using a 75gram oral glucose load, random glucose checks o Has this (HHNKS) Hyperosmotic, hypoglycemic non-ketotic syndrome, instead of DKA o Tx – IV insulin and IV fluids
  • Cushing’s disease - What two things are affected? Lose diurnal and circadian patterns of ACTH and cortisol secretion o Can you respond to stressors well? No, you do not increase ACTH/Cortisol secretion in response to stressor o Symptoms of cushing's disease? Truncal weight gain, moon face, buffalo hump Glucose intolerance, protein wasting, loss of collagen, purple striae, and easy bruising https://s3-us-west-2.amazonaws.com/secure.notion-static.com/c9183119-9cdb- 4c3b-93e8-429c4165ed27/ds00470_im00313_r7_cushingssyndromethu_jpg.webp
  • Endocrine Lab tests
  • Somogyi effect - What happens to your glucose ⬆ or ⬇ at 3am? What's the treatment? Who is it most common with? 3am = ⬇ glucose; Tx: ⬇ insulin or change the timing ; most common with DM type 1 Occurrence of hypoglycemia at about 3:00 AM caused by too much intermediate-acting insulin (that is, NPH insulin) given at dinner time followed by rebound hyperglycemia caused by normal early morning secretion of counter-regulatory hormones (epinephrine, growth hormone (GH), corticosteroids), which are stimulated by hypoglycemia and cause gluconeogenesis. Excessive carbohydrate intake may contribute to rebound hyperglycemia. The treatment is to decrease the evening insulin level. The Somogyi effect is becoming much less common because of the increasing use of long-acting bioengineered insulins.
  • Dawn Phenomenon: What happens to your glucose ⬆ or ⬇ at 3am? What's the treatment? Which hormone is it related to? Early morning glucose ⬆ , w/out noctornal hypoglycemia Related to growth hormone ⬆ Tx: Glucose check at 3am, if it's ⬆ , give more insulin or change the timing . **HEMATOLOGY AND CANCER
  • Enzyme telomerase and cancer** o Telomerase is commonly expressed in human cancer cells. Increased telomerase expression produces vulnerability of cancer cells, distinguishing them from normal cells in the body, although normal cells do also have some active telomerase. o The cancer cells activate the telomerase, so that the telomere's can reactivate the cancer cell, causing it the be "immortal" - cancer cells reactivate telomerase so that they CAN LIVE FOREVER

Cancer cells are characterized by high telomerase activity, which enables cells to divide indefinitely; they also avoid cell death This is possible because the cancer cells activate an enzyme called telomerase, which adds genetic units onto the telomeres to prevent them from shortening to the point of causing senescence or cell death. Telomerase is silenced in most normal cells but is active in an estimated 85% to 95% of human cancer cells. As a result, cancer cells essentially become immortal. - from google
Telomerase is a good biomarker for cancer detection because most human cancers cells express high levels of it. Telomerase activity can be identified by its catalytic protein domain (hTERT). This is the rate-limiting step in telomerase activity. It is associated with many cancer types.

  • Tumor cell markers. - IN THE TEST - which are the tumor markers for prostrate Ca? Breast Ca? Pheochromocytoma? Liver Ca? o Hormones, enzymes, genes, blood, spinal fluid, urine o PSA - prostate stimulating hormone, CA o CA125 = breast cancer/Ovarian CA o Catecholamines - pheochromocytoma o AFP - liver CA
  • Anemia: iron deficiency vs pernicious vs aplastic o Iron Deficiency - Do you have a macrocytic or microcytic anemia? Causes? Microcytic anemia, can also be thalassemia Causes: Dietary deficiency, impaired absorption, increase requirement, chronic blood loss ▪ Sx? Tx? ▪ Pallor, mucous membrane, palmar crease, glossitis – bald, fissured loss of papillae and flattening Oral Iron supplement o Pernicious Anemia - Do you have a macrocytic or microcytic anemia? Which vitamin is deficient? You have macroctyic (megaloblastic anemia) This is caused by a loss of intrinsic factor which is needed to absorb vitamin B Vit B12 insufficiency ▪ Sx? what happens to your tongue? what lab tests should you order? - pale, fatigue, HA, NVD, SOB, beefy red tongue, retest- CBC W/B12, schilling test, IF antibody test. o Aplastic Anemia - What's happening in the bone marrow and what 3 things are low? Autoimmune disease ALL 3 cell lines down ( RBC, WBC, and Platelets because of bone marrow suppression ) - Like Panctyopen ▪ Sx? Do you have fever? bleeding? Fatigues, inc. infections, pale skin, sob, nosebleed, bleeding gums, HA, fever dizziness ▪ Tx? Meds, bld transfusion, stem cell transplant. IDA (Fe deficiency) – Most common(Microcytic hypochromic) impaired erythrocyte production/Fe deficiency, High milk intake, low pro, women w/menses,

Anemia of chronic disease Anemia of chronic disease refers to having low levels of red blood cells as a result of autoimmune diseases (diseases in which the body’s immune system attacks joints and/or body organs) or other chronic illnesses. Chronic diseases are those that last longer than 3 months. This condition is also called anemia of inflammation or anemia of inflammation and chronic disease (AI/ACD). It is the second most common type of anemia, after anemia caused by a deficiency of iron. ▪ Manifestation of anemia fatigue, weak, pale skin, irregular heartbeats, dizziness, chest pain, cold hands/feet. please see above for different types of manifestations for aplastic, iron defiency, and pernicious anemia ▪ Hodgkins lymphoma Hodgkin's lymphoma — formerly known as Hodgkin's disease —A cancer of the immune system that develops from abnormal B-cells. It causes enlarged lymph nodes without pain in neck, armpits or groin, fever, fatigue, night sweats, and weight loss. It may affect people of any age, but is most common in people between 20 and 40 years old and those over 55. In Hodgkin's lymphoma, cells in the lymphatic system grow abnormally and may spread beyond it. Hodgkin's lymphoma is one of two common types of cancers of the lymphatic system. The other type, non-Hodgkin's lymphoma, is far more common. o Is the lymphoma all over the body? Where? Usually localized in one area, single group of nodules account for 10% o What are the symptoms of Hodgkins Lymphoma? Fever, NOC sweats, weight loss, neck painless lymph node elargement ▪ What about non-Hodgkins? NO FEVER, NO night sweats, and NO weight loss o Hodgkins vs Non-Hodgkin's (picture) - which one is the most common? which is more localized and which part of the body?

HIT - Heparin induced thrombocytopenia o Heparin-induced thrombocytopenia (HIT) is a potentially fatal immunologic complication of heparin therapy. o The cardinal clinical manifestations are a fall in the platelet count and an increased propensity for thromboembolism in the setting of a proximate heparin exposure. o Management involves immediate discontinuation of heparin and initiation of an alternate parenteral anticoagulant to prevent or treat thrombosis. ▪ DIC - Disseminated Intravascular Coagulation A condition where blood clots are excessively formed in the body's blood vessels. This causes rectal or vaginal bleeding, low blood pressure, and easy bruising. o What could be the underlying cause Sepsis, cancer o What happens? How are the labs affected? Platelets? short or long PT/PTT? ⬆ or ⬇ in plasma fibrinogen level? ⬆ or ⬇ in D d- dimer? Clots can cause organ failure Consumption of clotting factors lead to excessive bleeding ▪ Excessive bleeding ▪ Thrombocytopenia ▪ Prolonged PT/PTT ▪ Decline plasma fibrinogen level ▪ Elevated D-Dimer ▪ How does the body compensate from posthemorrhagic anemia o In acute blood loss anemia (post hemorrhagic), Will the numbers be normal? Where does erythropoietin get secreted? What will you see a rise in labs? Numbers will be normal- but the acute blood loss causes tissue hypoxemia which stimulates production of erythropoietin by the kidney and this increases production of erythrocytes and you will see a rise in reticulocytes. ▪ Pathophysiology of leukemias - what happens? Are malignant disorders of the blood and blood forming organs Exhibit uncontrolled proliferation of malignant leukocytes: overcrowds the bone marrow and there is a decreased production of function of normal hematopoietic cells o What are the classification? Myeloid or lymphoid o Acute lymphocytic Leukemia (ALL) is most common in who? Most common in childhood o Acute Myelogenous Leukemia (AML) is most common in who? Adults ▪ What is pancytopenia Pancytopenia is a relatively common hematological entity. It is a striking feature of many serious and life-threatening illnesses, ranging from simple drug-induced bone marrow hypoplasia, megaloblastic anemia to fatal bone marrow aplasias and leukemias. deficiency of all three cellular components of the blood ( red cells, white cells, and platelets ).

o Inherited disorder cause by a genetic defect in the RBC enzyme G6PD. o G6PD is first step of converting glucose to ribose -5-phosphate. o Leads to damaged RBC that rupture and bread down prematurely. o Occurs in tropical and subtropical regions of the Eastern Hemisphere, Europe, Africa and Asia. o X-linked recessive disorder o Sx – icterus neonatorum ( jaundice ) The symptoms of G6PD deficiency are: Fatigue, Paleness, Dark urine, Rapid heart rate, Shortness of breath, Heart murmur, Enlarged spleen and liver, Yellow skin and eyes o Tx – prevent hemolysis, avoid meds and dietary substances assoc w/ hemolysis o Dialysis: In case of kidney failure Splenectomy: May help some cases as spleen is the site of red cell destruction. IMMUNITY AND INFECTIOUS DISEASE Evasion and the Infectious Process What type of bacterium is associated with endotoxins Endotoxins are part of the outer membrane of the cell wall of Gram-negative bacteria. Endotoxin is invariably associated with Gram-negative bacteria whether the organisms are pathogenic or not. Although the term "endotoxin" is occasionally used to refer to any cell-associated bacterial toxin, in bacteriology it is properly reserved to refer to the lipopolysaccharide complex associated with the outer membrane of Gram-negative pathogens such as Escherichia coli, Salmonella, Shigella, Pseudomonas, Neisseria, Haemophilus influenzae, Bordetella pertussis and Vibrio cholerae. Lead to fatal endotoxic shock (septic shock) leading causes of death in ICU. Septicemia. o Release vasoactive peptides/cytokines, cause decrease o2 delivery and = cardiovascular shock o From PPT: ENDOTOXIN - Gram negative pyrogenic bacteria. - Chester Pathological invasion of viruses Pathogenesis is the process by which an infection leads to disease. Pathogenic mechanisms of viral disease include (1) implantation of virus at the portal of entry, (2) local replication, (3) spread to target organs (disease sites), and (4) spread to sites of shedding of virus into the environment. Factors that affect pathogenic mechanisms are (1) accessibility of virus to tissue, (2) cell susceptibility to virus multiplication, and (3) virus susceptibility to host defenses. Natural selection favors the dominance of low-virulence virus strains.

  • Gram-positive and gram-negative bacteria - which one has a thick cell wall? which one are endotoxins? Give examples of each Gram positive – exotoxins o Streptococcus P (A), B, D, strep pneumonia, staphylococcus A, C. Diff o Thick cell wall then plasma membrane

o Gram Negative – endotoxins o E. coli, H. Influenza, M. Gonorrhea, chlamydia o Outer membrane (releases endotoxins), small cell wall then plasma membrane Role of T cells and the immune system T cells (also called T lymphocytes) are major components of the adaptive immune system. Their roles include directly killing infected host cells, activating other immune cells, producing cytokines and regulating the immune response. T-cell receptors recognize peptides presented by the major histocompatibility complex (MHC) on the surface of antigen-presenting cells (APC). The ability of the T-cell receptor (TCR) to recognize more than one peptide-MHC structure defines cross-reactivity. T lymphocytes originate from haematopoietic stem cells within the bone marrow. Some of these multipotent cells subsequently become lymphoid progenitor cells that leave the bone marrow and travel to the thymus via the blood. Once in the thymus, T lymphocytes undergo a selection process in which the majority of developing T cells (called thymocytes) will not survive. During this process, thymocytes with receptors for self-antigens receive negative signals and are removed from the repertoire. Each T lymphocyte has a T cell receptor (TCR) which is specific to a particular antigen. T lymphocytes that survive thymic selection will mature and leave the thymus. After that, They circulate through peripheral lymphoid organs, ready to encounter their cognate antigens and become activated. The thymus atrophies as we age and so produces fewer naïve T lymphocytes over time.

  • If a person was deficient in T cells what woud you worry about? What do T cells do? from PPT: T cells are produced by the thymus and are cell-mediated – they usually hunt down and kill cancer cells so a decrease in your T cells makes you more susceptible to opportunistic infections. Vaccinations and how they protect Vaccination is the administration of a vaccine to help the immune system develop protection from a disease. Vaccines contain a microorganism or virus in a weakened, live or killed state, or proteins or toxins from the organism. In stimulating the body's adaptive immunity, they help prevent sickness from an infectious disease. When a sufficiently large percentage of a population has been vaccinated, herd immunity results. Herd immunity protects those who may be immunocompromised and cannot get a vaccine because even a weakened version would harm them. The effectiveness of vaccination has been widely studied and verified. Vaccination is the most effective method of preventing infectious diseases; widespread immunity due to vaccination is largely responsible for the worldwide eradication of smallpox and the elimination of diseases such as polio and tetanus from much of the world. However, some diseases, such as measles outbreaks in America, have seen rising cases due to relatively low vaccination rates in the 2010s — attributed, in part, to vaccine hesitancy. Mother to baby passive immunity
  • The newborn's immune system grows fast from a small size at birth by exposure primarily to the intestinal microflora normally obtained from the mother at and after birth. While building up its immune system, the infant is supported by the transplacental IgG antibodies, which also contain anti-idiotypic antibodies, possibly also actively priming the offspring. The second mode of transfer of immunity occurs via the milk. Numerous major protective components, including secretory IgA (SIgA) antibodies and

C. directing leuckocytes to the inflamed area : two chemotactic factors, neutrophil chemotactic factor (NFC) and eosinophil chemotactic factor of anaphylaxis (ECF- A), are released druing mast cell cell degranulation.

  • What is opsonization in the inflammatory process phagocytes recognize and adhere to bacteria This is part of the complement pathway - The process at which opsonins bind to the surface of the antigen so that the antigen will be readily identified and engulfed by phagocytes for destruction - google o from quizlet: Which component of plasma protein system tags pathogenic microorganisms for destruction of neutrophils and macrophages? A. complement cascade system - C3b adheres to the surface of a pathogenic microorganism and serves as efficient opsonin. opsonins are molecules that tag microorganisms for destruction by cells of the inflammatory system, primarily neutrophils and macrophages. o from quizlet: what is the outcome of the complement cascade? Answer: lysis of bacterial cell membranes o from quizlet : o Answer A. Phagocytes How does swelling occur in inflammation ( GOOGLE) When an inflammation occurs in your body, many different immune system cells may be involved. They release various substances, known as inflammatory mediators. These include the hormones bradykinin and histamine. They cause the small blood vessels in the tissue to become wider (dilate), allowing more blood to reach the injured tissue. For this reason, inflamed areas turn red and feel hot. The increased blood flow also allows more immune system cells to be carried to the injured tissue, where they help with the healing process. What’s more, both of these hormones irritate nerves and cause pain signals to be sent to the brain. This has a protective function: If the inflammation hurts, you tend to protect the affected part of the body. The inflammatory mediators have yet another function: They make it easier for immune system cells to pass out of the small blood vessels, so that more of them can enter the affected tissue. The immune system cells also cause more fluid to enter the inflamed tissue, which is why it often swells up. The swelling goes down again after a while, when this fluid is transported out of the tissue. Mucous membranes also release more fluid when they are inflamed. For instance, this happens when you have a stuffy nose and the membranes lining your nose are inflamed. Then the extra fluid can help to quickly flush the viruses out of your body.
  • from quizlet: What causes edema that occurs during the inflammatory process? increased capillary permeability
  • Hypersensitivity reaction type III Antigen/antibody complex in plasma deposited into tissues examples: Lupus, Reynaud's
  • Types of hypersensitivity - which is IgE mediated? Which is NOT antigen- related? which is where plasma is deposited into tissues? Type 1 - IgE mediated - allergies Type 2 - antigen / antibody reaction on surface marker Type 3 antigen / antibody complex in plasma deposited in tissues Type 4 not - antigen related - Delayed T cell mediated
  • What causes fever in the inflammatory process A fever is an inflammatory response that extends beyond the site of infection and affects the entire body, resulting in an overall increase in body temperature. Body temperature is normally regulated and maintained by the hypothalamus, an anatomical section of the brain that functions to maintain. However, certain bacterial or viral infections can result in the production of pyrogens, chemicals that effectively alter the “thermostat setting” of the hypothalamus to elevate body temperature go I and cause fever. Pyrogens may be exogenous or endogenous. For example, the endotoxin lipopolysaccharide (LPS), produced by gram-negative bacteria, is an exogenous pyrogen that may induce the leukocytes to releas e endogenous pyrogens such as interleukin-1 (IL-1), IL-6, interferon-γ (IFN-γ), and tumor necrosis factor (TNF). In a cascading effect, these molecules can then lead to the release of prostaglandin E2 (PGE2) from other cells, resetting the hypothalamus to initiate fever (Figure 4). - from google From quizlet: fever is caused by cytokines that are known as endogenous pyrogens. These pryogens act directlyl on the hypothalamus, which is the portion of the brain that controls the body's thermostat. The other options do not accurately describe the cause of fever related to the effects of the hypothalamus.
  • Type 4 sensitivity reaction - is it antigen related? Which cell is mediated? Type 4 is not antigen related - delayed T cell mediated
  • Chronic effects of glucocorticoids during stress Glucocorticoid receptors are a type of receptors on the outside of cells that transmit signals from glucocorticoids, such as cortisol. Poor glucocorticoid receptor function due to chronic stress and high CRH can lead to cortisol resistance, possibly increasing inflammation, autoimmunity, and weight gain. Long term effects from elevated cortisol (glucocorticoid) will mimic that of elevated glucose Anxiety can elicit the SNS response from google: Major depression and anxiety disorders o Which hormone is the stress hormone? Cortisol
  • What immunoglobulins is found in body secretions IgG, IgM, IgA In normal serum, about 80% is immunoglobulin G (IgG), 15% is immunoglobulin A (IgA), 5% is immunoglobulin M (IgM), 0.2% is immunoglobulin D (IgD), and a trace is immunoglobulin E (IgE). from google IgG - 80% found in blood, most abundant, cross placental barrier IgM - blood, lymph/ mucosal surfaces - IgM is the FIRST responder in ACUTE infections

o What is the difference between stable and unstable angina? how is stable angina relieved? stable angina is predictable and relieved with usually interventions nitro, rest unstable angina has plaque progression, disruption, and subsequent clot formation. May not have signs of heart attack on their ECG or blood tests. o T/F Myocardial ischemia is NOT reversible False, it is reversible, it is myocardial infarction that is NOT reversible

  • Myocardial ischemia o Myocardial infarction - NSTEMI vs STEMI - are troponin increased in NSTEMI? In NSTEMI, what do you see on the EKG? NSTEMI -no elevation but you see that troponin has ⬆ ; usually presents with ST Depression and T wave inversion
  • EKG findings after a myocardial infarction ST segment elevation.
  • Pericarditis inflammation of pericardium - is this an emergency? o it is acute - most common affecdting pericardium, this is an EMERGENCY - how do you treat? Meds: Pain relievers, colchicine, corticosteroids Surgery: pericardiocentesis o what kind of chest pain do you get? associated with anterior chest pain that worsens with respiratory effort, tx with corticosteroids o Is this the result from an MI? When MI heals, acute pericarditis may develop
  • Venous thrombus Deep vein thrombosis (DVT) is a medical condition that occurs when a blood clot forms in a deep vein. These clots usually develop in the lower leg, thigh, or pelvis, but they can also occur in the arm. A blood clot in a deep vein, usually in the legs. This condition is serious because blood clots can loosen and lodge in the lungs. Leg pain or swelling may occur, but there may be no symptoms. Treatments include medications and the use of compression stockings. o What is the sign that you look for to test for DVT? Homan's Sign - Bending the calf when bending the foot up while supine o what else can develop? PE
  • Murmurs: AS, MR, MVP o Aortic Stenosis - which valve can't open fully? where does it radiate to? inability of the aortic valve to open fully; radiates to NECK you will hear a diastolic murmur o Mitral Regurgitation - permits backflow from what to what? what type of pressure does it ⬆? permits backflow of blood from L ventricle into left atrium; ⬆ atrial pressure, also caused by pulmonary HTN and R ventricular failure; radiates to axilla Cardinal sign: Mitral regurgitation is a holosystolic murmur , heard best at apex

o Mitral valve prolapse - what kind of murmur do you hear? from quizlet - late systolic murmur usually preceded by mid-systolic click heart problem resulting from the mitral vale not regulating the flow of blood between the L atrium and L ventricle of the heart. Sx: atypical chest pain, palpitations, fatigue, anxiety, dypnea on exertion, hypotension and you hear a mild systolic ejection CLICK at the apex of the heart. ▪ Questions from quizlet about murmurs question: atypical chest pain, palpitations, fatigue, anxiety, dyspnea unrelated to exertion, hypotension, mild systolic ejection CLICK at apex. which murmur would you suspect Mitral valve prolapse ▪ Question: On auscultation, you hear a harsh blowing pansystolic murmur at the apex, what is the most likely diagnosis? Mitral regurgitation

  • Systolic vs. diastolic dysfunction o which is more common? Systolic dysfunction is more common; o What happens in diastolic dysfunction? Also called "restrictred cardiomyopathy," diastolic dysfunction is the impaired ability of ventricles to fill. Why? B/c the heart does not have much blood to eject
  • Cardiac dysrhythmias: AF most prevalent cardiac arrhythmia The loss of atrial systole and the irregular, fast heart rate contribute to symptoms such as palpitations and ⬇ exercise tolerance and also predispose to the development of intracardiac thrombus and systemic thromboembolism Most common cardiac rhythm disorder, impulses in the heart become disorganized leading to a rapid and irregular heart rhythm. Atrial electrical is activity irregular and atrial contraction is ineffective. QRS – rapid irregular ventricular response and impaired pump function.
  • Lab testing for CHF o B-type natriuretic peptide (BNP) or N-terminal pro-BNP—measure the concentration of a hormone produced by the left ventricle (the main pumping chamber of the heart) to help diagnose and grade the severity of heart failure o Metabolic panel —to check for electrolyte imbalance, kidney failure (since symptoms of kidney disease are similar to those of CHF) and liver disease o Complete blood count (CBC) —to check for anemia, which can cause similar symptoms to CHF as well as contribute to CHF o Thyroid tests —these tests check the level of thyroid hormone in the blood; both hyperthyroidism (too much thyroid hormone) and hypothyroidism (too little thyroid hormone) can cause heart failure.
  • Electrical conduction in the heart SA NODE (60-100) —> AV NODE —> bundle of HIS —-divides→R and left pathways bundle branches to stimulate R and Left ventricles
  • Long term complications from HTN

Can cause – aortic aneurysm, aortic dissection, valve malformation Eye – lens dislocation, retinal problems, enarly onset glaucoma Tx Treatment usually includes medications to keep your blood pressure low to reduce the strain on your aorta. Regular monitoring to check for damage progression is vital. Many people with Marfan syndrome eventually require preventive surgery to repair the aorta.