NURS 548: Patho Midterm Questions and Answers Latest updated
Apoptosis
● Cell death
● They do not die off (apoptosis) to keep the number of total
... [Show More] cells consistent
Cell Cycle- Which category does the cell fit into?
● Labile Cell
○ These cells must divide continually to replace cells that are constantly being depleted by normal processes.
○ Never in the G-0 phase (M-phase).
○ Constantly going through cell cycle
● Permanent Cell
○ Cells that cannot undergo mitosis.
○ Stuck in the G-0 phase
○ hypertrophy but no hyperplasia
● Stable Cell
○ Cells that do not regularly undergo mitosis but are able to if the need arises.
○ Also in the G-0 phase but can reenter the cell cycle.
○ Hypertrophy and Hyperplasia
Proto-Oncogenesis- Generalized question
● normal cellular genes that are important regulators of normal cellular processes, they promote growth. alterations in the expression of these cells result in oncogenes
○ Growth factors
○ Growth factor receptors
○ G proteins
○ Enzymes that produce second messengers
○ Genes that turn the production of these proteins on and off
● A normal gene which, when altered by mutation, becomes an oncogene that can contribute to cancer. Proto-oncogenes may have many different functions in the cell. Some proto-oncogenes provide signals that lead to cell division. Other proto- oncogenes regulate programmed cell death (apoptosis).
● The defective versions of proto-oncogenes, known as oncogenes, can cause a cell to divide in an unregulated manner. This growth can occur in the absence of normal growth signals such as those provided by growth factors. A key feature of oncogene activity is that a single altered copy leads to unregulated growth.
Oncogenesis- What occurs at each stage?
● Formation of cancer cells.
● Initiation: initial mutation occurs
● Carcinogenic agent (chemicals, radiation, viruses), DNA damage and cell mutation lead to mutated cells
● Promotion: mutated cells are stimulated to divide
○ Activation of oncogenes by promoter agent
● Progression: tumor cells compete with one another and develop more mutations which make them more aggressive
○ Malignant tumor
Naming Scheme for Tumors- identify if benign or malignant and originating tissue
● Benign Tumors: Tissue + “oma”
○ Fibroma: connective tissue
○ Lipoma: slow-growing fatty tumor located between the skin and muscle layer
○ Osteoma: tumor of the bone
○ Papilloma: epithelial tumor
● Malignant Tumors (cancers)
○ Epithelial tissue: tissue name + “carcinoma”
■ Squamous cell carcinoma, bronchogenic carcinoma
○ Mesenchymal tissue: tissue name + “sarcoma”
■ Fibrosarcoma, liposarcoma, osteosarcoma
Acute Inflammation- Primary function of prostaglandins and leukotrienes effects on blood vessels
● Primary function of prostaglandins in vascular stage of inflammation
○ build and repair tissues and structures
○ Prostaglandins increase the effects of other substances that promote vascular permeability.
○ prostaglandins are associated with the pain and fever of inflammation.
● Primary function of leukotrienes in vascular stage of inflammation
○ Prostaglandins are synthesized from arachidonic acid, as are the leukotrienes, another group of chemical mediators that have vasoactive properties.
● These products are both potent vasodilator and hyperalgesic agents and since they have been detected at sites of inflammation it is believed that they contribute to erythema, oedema and pain which are characteristic of the inflammatory response. Prostaglandin E2 is also a power
Kinds of Exudate- given characteristic, identify type
● Serous:clear fluid that seeps out of the tissues.
● Hemorrhagic: Bloody Contains blood, indicates bleeding; composed of erythrocytes
● Fibrinous: Contains fibrin
● Membranous: mucous membrane surfaces i.e thrush(oral cavity, patches of membranous)
● Purulent: Pus filled and debris
Leukocytes Entering Injured Area- Processes occurring during pavementing,
emigration, chemotaxis
● Pavementing: adherence of white blood cells (neutrophils) to the walls of a blood vessel during inflammation
● Emigration: neutrophils migration from a location into the affected area
● Chemotaxis: chemical attraction causing neutrophils to infected area of tissue
○ Phagocytosis
Leukocytes Release Inflammatory Mediators- Function of Histamine and Serotonin
● What are two examples of vasoactive amines?
○ Allow for dilation of arterioles
○ Allow for permeability of venules
● Histamine: a chemical released by the body during an inflammatory response that causes blood vessels to dilate
● Serotonin: vasoactive mediator similar to histamine found in mast cells and platelets in the GI tract and CNS.
○ Increases vascular permeability, dilates capillaries, and causes contraction of nonvascular smooth muscle
Chronic Inflammation- Granulomatous Chronic Inflammation
● Macrophages mass together around foreign bodies
● Connective tissue surrounds and isolates the mass
● Associated with foreign bodies (splinters, sutures, silica, asbestos) and with microorganisms that cause tuberculosis, syphilis, sarcoidosis, deep fungal infections, and brucellosis
● Type of inflammation characterized by a special tissue reaction where the participating cells are reticuloendothelial cells and their derivatives, largely macrophages. It is an attempt to wall-off and isolate the affected site.
Mechanisms of Fever- Known Entire Diagram
Manifestations of
Fever- 2 Q’s( 1 on stages, 1 on Manifestations)
● Successive Stages of Fever
○ Predromal Period: characterized by nonspecific complaints
○ Chill Stage: temp raising, characterized by sensation of being chilled, with generalized shaking
○ Flush Stage: characterized by cutaneous vasodilation and warm and flushed skin
○ Defervescence Stage: characterized by sweating
● Common Manifestations of Fever
○ Anorexia, myalgia(soreness), arthralgia (joint pain), fatigue
○ Respirations increased, heart rate usually elevated
○ Dehydration may occur due to sweating and rapid resp rate
● Mechanisms of a Fever
○ Pyrogens (Prostaglandins E1)
○ Resetting of thermostatic set point
■ sent to the hypothalamus( thermostatic set point)
○ Temperature raising response
■ shivering , vasoconstriction, piloerection, increased metabolism
○ Then you have the fever - core body temp reaches new set point ( back at the hypothalamus)
○ Temperature reducing response
Classifications of Hypersensitivity Response- mechanism given, identify hypersensitivity
● Type I: Immediate Hypersensitivity
○ IgE mediated - mast cell degranulation
○ ex. hay fever, asthma, anaphylaxis
● Type II: Antibody-Mediated Hypersensitivity
○ Formation of antibodies ( IgG, IgM) against cell surface antigens
○ Complement is usually involved.
○ ex. autoimmune hemolytic anemia, hemolytic disease of the newborn, GoodPasture Disease
● Type III: Immune Complex-Mediated Hypersensitivity
○ Formation of antibodies (IgG, IgM, IgA) that interact exogenous and endogenous antigens to form antigen
○ antibody complexes that cause vessel or tissue injury
○ ex. arthus reaction, autoimmune diseases (lupus, rheumatoid arthritis, erythematous) , certain forms of acute glomerulosclerosis
● Type IV: Cell-Mediated Hypersensitivity
● Type IV Hypersensitivity
○ Sensitive T-lymphocytes release cytokines that cause direct cell mediated cytotoxicity, or delayed type hypersensitivity
○ ex. TB, contact dermatitis, transplant rejection
Anaphylaxis- Entire Slide Generalized
● Acute allergic response to an antigen that results in severe hypotension and may lead to life-threatening shock if untreated.
● Systemic response to the inflammatory mediators released in Type I hypersensitivity
● Histamine, acetylcholine, kinins, leukotrienes, and prostaglandins all cause vasodilation
○ What will happen when arterioles vasodilate throughout the body?
● Acetylcholine, kinins, leukotrienes, and prostaglandins all can cause bronchoconstriction
○ What will happen when the bronchioles constricted
Mechanism of Autoimmune Diseases- Entire Slide Generalized
● Gender
○ A number of autoimmune diseases occur more commonly in women than in men
● Genetic Susceptibility
○ Several autoimmune diseases exhibit familial clustering
● Environmental Factors
○ Breakdown in T-Cell Anergy - lack of reaction by the body's defense mechanisms to foreign substances, and consists of a direct induction of peripheral lymphocyte tolerance.
○ Release of Sequestered Antigens -those that can not interact with the immune system during development as they are anatomically sequestered and hence lymphocytes specific for such sequestered antigens are not deleted. These are treated as foreign when introduced into the circulation, and elicit both humoral and cellular responses.
○ Molecular Mimicry - Antigens of certain bacteria and viruses mimic (resembles) self-antigens
○ Superantigens - are a class of antigens that cause non-specific activation of T-cells resulting in polyclonal T cell activation and massive cytokine release. SAgs can be produced by pathogenic microbes (including viruses, mycoplasma, and bacteria) as a defense mechanism against the immune system.
Course of HIV Infection: Know Entire Slide
● Primary Infection Phase
○ Signs of systemic infection
○ Seroconversion: immune system responds and antibodies against HIV appear (1-6 months)
● Latent Period
○ Second stage
○ Virus is replicating, T helper count gradually falls.
○ May last 10-11 years or longer
● Overt AIDS
○ stage 3
○ T helper cell count is <200 cells/mL or AIDS-defining illness
White Blood Cells/Leukocytes- Know types of lymphocytes
● B Cells:a white blood cell that makes antibodies
● T Cells: control immune response; cell-mediated immunity
● Natural Killer Cells: kill antigenic cells
Clinical Manifestations of Leukemia
● Bone Marrow Depression
○ Malaise, fever, bleeding (petechiae, ecchymosis, gingival bleeding, epistaxis)
● Bone pain and tenderness upon palpation
● Headache, nausea, vomiting, papilledema, cranial nerve palsies, seizures, coma
● Abdominal discomfort
● Increased vulnerability to infections
● Hematologic abnormalities
○ Anemia, thrombocytopenia
● Hyperuricemia and other metabolic disorders
● nausea, vomiting, weight loss, pain, fatigue, weakness, neurologic complications
Four Types of Leukemia- characteristic given, identify type
● Acute Lymphocytic Leukemia (ALL)
○ Most common leukemia in childhood
○ peak incidence = 2-4 years of age
● Acute Myelogenous Leukemia (AML)
○ Chiefly an adult disease, but also seen in children and adolescents
○ Type of leukemia associated with Down's syndrome
● Chronic Lymphocytic Leukemia (CLL)
○ Mainly a disorder of older persons
○ Men are affected twice as often as women
● Chronic Myelogenous Leukemia (CML)
○ Predominantly a disorder of adults between the ages of 30 and 50 years
○ Incidence is slightly higher in men than women
○ Associated with the presence of the Philadelphia chromosome
Lymphomas- known hallmarks of Hodgkins v. Non-Hodgkins
● Hodgkin’s Lymphoma
○ Reed-Sternberg cells
○ Malignant B cells invade lymphoid organs
● Non-Hodgkin’s Lymphoma
○ Malignant tumors of immune system -B cells
○ B cell
○ T cell
Platelet- identify incorrect statement
● Platelets live 8-9 days in circulation
● Many are stored in spleen
● Released when needed
Intrinsic and Extrinsic Coagulation Pathways- Know Blue Box
●
● Prothrombin - Thrombin -Ca fibrinogen- Fibrin (Monomer) - Fibrinin (Polymer)
Fate of Bilirubin- General Question about Steps
● Unconjugated bilirubin has not been processed by the liver and is toxic
● Causes Bilirubenemia - then jaundice
● liver links it to gluconoride- turns to conjugated bilirubin- turns into bile
● Why would a man with liver failure develop jaundice?
Sickle Cell Disease- Identify incorrect statement
● A disease that causes the RBCs to be misshapen, resulting in poor oxygen- carrying capability and potentially resulting in lodging of the RBCs in blood vessels or the spleen.
● Mutation in beta chains of hemoglobin
● When hemoglobin is deoxygenated, beta chains link together
● Forming long protein rods that make the cell "sickle"
● Sickle cell anemia is an inherited form of anemia — a condition in which there aren't enough healthy red blood cells to carry adequate oxygen throughout your body.
● Normally, your red blood cells are flexible and round, moving easily through your blood vessels. In sickle cell anemia, the red blood cells become rigid and sticky and are shaped like sickles or crescent moons. These irregularly shaped cells can get stuck in small blood vessels, which can slow or block blood flow and oxygen to parts of the body.
Hemolytic Anemia- Inherited Disorders of RBC Membrane
● Hereditary Spherocytosis- autosomal dominan
○ People with this condition typically experience a shortage of red blood cells (anemia), yellowing of the eyes and skin (jaundice), and an enlarged spleen (splenomegaly).
Polycythemia- relative polycythemia
● ↓ plasma volume; ↑ RBC count; normal RBC mass
○ Due to a loss of plasma volume without a corresponding decrease in red blood cells
○ Occurs with water deprivation, excess use of diuretics, or GI losses
○ Corrected by increasing the vascular fluid volume
● Relative polycythemia describes conditions in which red cell volume is high due to increased blood concentration of red cells as a result of dehydration. In these situations (vomiting, diarrhea, excessive sweating) the number of red blood cells is normal, but because of the fluid loss affecting the blood (plasma), red blood cell counts may seem elevated.
Lipid Transport in the Body- Know Entire Slide
● IDLs become low-density lipoproteins ("bad cholesterol")
● These can deliver fat to the liver and to other tissues
● LDL receptors are necessary for the liver to take them up
● Some LDLs are taken up by scavenger cells like macrophages
● High-density lipoproteins ("good cholesterol") are made in the liver
○ They go out to the peripheral tissues and pick up lipid
○ Then they carry it back to the liver
●
Proposed Pathogenesis of Atherosclerosis- Identify incorrect statement
● The response to injury hypothesis of plaque formation proposes that injury to the endothelial vessel layer is the initiating event in the development of atherosclerosis
● Possible injurious agents include products associated with smoking, immune mechanisms, and mechanical stress, such as that associated with hypertension
● Hemodynamic factors are thought to play a role because the atherosclerotic lesions tend to form where vessels branch or where there is turbulent blood flow
● Hyperlipidemia is believed to play an active role in the pathogenesis of the atherosclerotic lesion
● Activated macrophages may play a role by releasing free radicals that oxidize LDL (oxidized LDL is toxic to the endothelium)
● Activated macrophages ingest oxidized LDL to become foam cells
Stable Atherosclerotic Plaques- Know characteristics
● Have thick, fibrous caps
● Partially block vessels
● Do not tend to form clots or emboli
Disorders of Arterial Circulation- Thromboangitis Obliterans (Berger’s Disease)
● Rare inflammatory occlusive disease of the medium sized and small arteries and veins
● inflammatory disease that affects the peripheral arteries that is mainly due to smoking and lead to amputation of the limbs
Aneurysms and Dissections- Familiarize with Diagram Types
● Wall of artery weakens and stretches
● Risk of rupture and hemorrhage
● Risk of clot formation
● Berry Aneurysm:A small saccular congenital aneurysm of a cerebral vessel is called?
● Descending Aneurysm:
● Abdominal Aortic Aneurysm:An aneurysm that is below the renal arteries and above the bifurcation of aorta.
○ Caused by HTN and smoking
○ pulsations can be felt
Renin-Angiotensin-Aldosterone System- Identify incorrect statement
● A reduction in arterial blood pressure stimulates the release of renin by the kidneys into the blood
● Renin catalyzes the conversion of angiotensinogen to angiotensin I in the plasma
● Angiotensin I is converted to Angiotensin II by ACE in the lungs
● Angiotensin II triggers the vasoconstriction of systemic arterioles
● Angiotensin II stimulates the adrenal cortex to secrete - - aldosterone, which stimulates the kidneys to reabsorb sodium
● Sodium reabsorption leads to an increase in arterial blood pressure
●
Malignant Hypertension- Know entire slide
● A small number of patients with secondary hypertension develop an accelerated and potentially fatal form of the disease - Malignant Hypertension
● Characterized by sudden marked elevation of blood pressure, renal disorders, vascular changes, and retinopathy
● Intense arterial spasm of the cerebral arteries may cause hypertensive encephalopathy
● Hypertensive crisis may ensue
Mechanisms of Orthostatic Hypotension- Know entire slide
● Causes
○ Reduced blood volume
○ Drug-induced hypotension
○ Aging
○ Bed rest and immobility
○ Disorders of autonomic nervous system function
○ Autonomic failure
○ Parkinson disease
○ Shy-Drager syndrome
● Assumption of Upright Position
○ Pooling of blood in the lower extremities
■ Decreased venous return to the heart→ decreased cardiac output→ drop in blood pressure → triggers baroreceptors
○ Activation of Skeletal Muscle Pumps
■ Compression of Veins→ Increased venous return→ increased cardiac output
○ Baroreceptors
■ Increased heart rate→ increased cardiac output→ BP returns to normal
■ Vasoconstriction causes BP to return to normal
●
Varicose Veins- Identify Incorrect Statement
● Varicose, or dilated, tortuous veins of the lower extremity are common and often lead to venous insufficiency
● Primary varicose veins arise in the superficial saphenous veins; secondary varicose veins result from impaired flow in the deep veins
● 80-90% of venous blood from the extremities flows through the deep veins
● The most common cause of secondary varicose veins is deep vein thrombosis (DVT)
● Other causes of varicose veins include congenital or acquired arteriovenous fistulas, congenital venous malformations, and pressure on the abdominal veins caused by pregnancy or a tumor
Venous Thrombosis (Thrombophlebitis)- Deep Vein Thrombosis
● Deep vein thrombosis of the lower extremity is a serious condition, complicated by pulmonary embolism, recurrent episodes of DVT, and development of chronic venous insufficiency
Pericarditis- Know entire slide
● Inflammation of the pericardium causes:
○ Pain
○ Exudate
■ Serous → pericardial effusion
● Cardiac tamponade: rapid accumulation of exudate compresses the heart
■ Fibrous friction rub; adhesions
○ ECG changes
Pulsus Paradoxus- Entire Slide
● During cardiac tamponade, the right ventricle fills with extra blood on inhalation
● he left ventricle is compressed both from without by fluid in the pericardium and from within by movement of the interventricular septum
● Because the heart cannot expand fully and the right ventricle is overfilling, the left ventricle cannot accept much blood
● On the next heartbeat, the left ventricle will not send out much blood: systolic BP drops
Acute Coronary Syndrome- ECG Changes
● T-wave inversion
● ST-segment depression or elevation
● Abnormal Q wave
Acute Myocardial Infarction (AMI)- Know manifestations
● Chest pain (unstable angina)
○ Severe, crushing, constrictive OR like heartburn
● Sympathetic nervous system response
○ GI distress, nausea, vomiting
○ Tachycardia and vasoconstriction
○ Anxiety, restlessness, feeling of impending doom
● Hypotension and shock
○ Weakness in arms and legs
Rheumatic Heart Disease- Identify incorrect statement
● Rheumatic Heart Disease is primarily a disease of school-aged children, with the peak incidence between 5 and 15 years of age
● Occurs as part of Rheumatic Fever, an acute, immune-mediated, multisystem inflammatory disease, involving connective tissue elements of the heart, blood vessels, joints, and subcutaneous tissues
● Most serious consequence of rheumatic fever is the development of chronic valvular disorders which can sometimes lead to fatal heart failure years later
Shunts Are Normal Before Birth- Know entire slide
● Foramen Ovale: Lets blood go from the right atrium to the left atrium to bypass the lungs
● Ductus Arteriosus: Lets blood go from the pulmonary trunk to the aorta to bypass the lungs
● Ductus Venosus: Lets blood go from the visceral veins to the vena cava, bypassing the liver
Compensatory Mechanisms of Heart Failure- Know entire slide(says will be “easy”)
● increase sympathetic(temporary) renin angiotensin gets bigger(long term vasoconstriction increase circulating vol)
● increase antidiuretic hormone(increase circulating vol)
● Sympathetic Nervous System (SNS)
● Renin -Angiotensin - Aldosterone System
● (RAAS)
● Antidiuretic hormone (Vasopressin)
●
Heart Failure Diagram- Right Sided Heart Failure
● Congestion of Peripheral tissue
○ Dependent edema and ascites
○ Liver congestion → Signs related to impaired liver function
○ GI tract congestion → Anorexia, GI distress and weight loss
Cardiogenic Shock- Manifestations
● Heart fails to pump blood adequately-when the heart is unable to pump as much blood as the body needs
○ Decreased cardiac output lowers BP
○ Sympathetic system responds
○ Vasoconstriction increases resistance to blood flow
○ Increased workload on heart worsens heart failure
Distributive or Vasodilatory Shock- Know entire slide
● Blood vessels dilate
● There is not enough blood to fill the circulatory system
● Blood flow decreases
● Less blood is returned to the heart
● Less blood is circulated to the body
Disseminated Intravascular Coagulation (DIC)- Know entire slide
● coagulation pathways activated
○ clots in many small blood vessels
■ microinfarcts and anemia
○ Platelets and clotting proteins used up
■ bleeding problems [Show Less]