Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Pathophysiology > Patho Exam #2 > Flashcards

Patho Exam #2 Flashcards

1
Q

Lymph nodes

A

 Part of the immune and hematologic systems
o Facilitates maturation of lymphocytes
o Transports lymphatic fluid back to the circulation
o Cleanses the lymphatic fluid of MOs and foreign particles

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Evaluation of the Hematologic System

A 
•	Tests of bone marrow function
	Bone marrow aspiration
	Bone marrow biopsy
	Measurement of bone marrow iron stores
	Differential cell count
•	Blood tests
	Large variety of tests – CBC
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Aging and the Hematologic System

A

• Erythrocyte lifespan is normal, but are replaced more slowly
 Possible causes
o Iron depletion
o Decreased total serum iron, iron-binding capacity, and intestinal iron absorption
 Lymphocyte function decreases with age
 Humoral immune system is less responsive

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Quantitative disorders

A

 Increases/decreases in cell numbers
o Leukopenia
 Not normal and not beneficial
 Low WBC predisposes a patient to infection
o Leukocytosis
 Normal protective physiologic response to physiologic stressors
 Bone marrow disorders or premature destruction of cells
 Response to infectious MO invasion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Qualitative disorders

A

 Disruption of cellular function

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Neutropenia

A

• Reduction in circulating neutrophils
• Causes
 Prolonged severe infection
 Decreased production caused by chemotherapy
 Reduced survival
 Abnormal neutrophil distribution and sequestration

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Leukemias

A

• Malignant disorder of the blood and blood-forming organs (Hematopoietic stem cells)
• Excessive accumulation of leukemic cells
 In bone marrow mutation
 Excessive accumulation of lymphocytic – B, T, or NK cells
 Excessive accumulation of myelogenous – monocytes or granular leukocytes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Acute leukemia

A

 Presence of undifferentiated or mature cells, usually blast (leukoblast) cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Chronic leukemia

A

 Predominant cell is mature but does not function normally

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Leukemia Symptoms

A

• Related to suppressed bone marrow function
 Infection – severe and/or recurrent
 Night sweats, fever, lymphadenopathy
 Anemia, pallor, fatigue, weight loss
 Nose bleeds, bleeding gums, petechiae (small red or purple spot caused by bleeding into the skin), ecchymosis (bruise)
• Related to infiltration to other organs with immature cells
 Enlarged spleen, liver, lymph nodes, bone and joint pain
 CNS symptoms (ALL & AML): headache, nausea, vomiting

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Leukemia Diagnosis

A

• Abnormalities in Complete blood cell count (CBC)
• X rays
• Bone marrow aspiration reveals leukemic blast cells and tumor markers
 Syringe is used to suck marrow from the iliac crest or the sternum
 Procedure used to examine bone marrow cells
• Lumbar puncture

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Chemotherapy

A

 Needs to be systemic
 Goal is to rid body of leukemic cells without completely destroying bone marrow
 Bone marrow transplant provides cure for some types of leukemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Acute Lymphocytic Leukemia (ALL) & Acute Malloid Leukemia (AML)

A

 Induction Therapy
o Intense combo of chemotherapy and radiation
o Given at time of diagnosis
o Goal to achieve remission
 Consolidation Therapy
o Given once remission achieved
o Variation of chemotherapy given during induction
o Curative intent; may be one treatment or repeated cycles for 1 – 2 years
o CNS treatment in children
 Maintenance Therapy
o Purpose to maintain remission
o Decreased dose of chemotherapy
o Usually given in cycles over several years (2-5)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Chronic Malloid Leukemia (CML)

A

 Chemo agents – administered orally
 In blast crisis
o Drugs similar to those used in AML
 Leukapheresis (WBCs are separated from a sample of blood), plateletpheresis (platelets are separated from a sample of blood)
 Bone marrow transplant before blast crisis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Chronic Lymphocytic Leukemia (CLL)

A

 Goal – palliation (make a disease or its symptoms less severe or unpleasant without removing the cause)
 Oral chemo agents to control WBC count

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Malignant Lymphomas

A

• Uncontrolled proliferation of lymphocytes arising from lymphoid tissues
• Invade bone marrow and other organs
Hodgkin’s Lymphoma
Non-Hodgkin’s Lymphoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Hodgkin’s Lymphoma (Disease)

A

 Associated with Epstein-Barr Disease (EBV)
 Form of lymphoma demonstrating the Reed-Sternberg cell, seen after doing a biopsy on a patient’s lymph node]
 Bimodal incidence peak
o Teens to mid-twenties or after 50
 Thought to be associated with inflammatory reaction to infectious agent, virus – EBV
 Painless progression of single node or group of nodes; spreads in continuous pattern
 Usually good prognosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Non-Hodgkin’s Lymphoma:

A

 Linked with chromosomal translocation
 Worst type
 Heterogeneic group of neoplastic disorders of lymphoid tissue; absence of Reed-Sternberg cell
 More prevalent than Hodgkin’s Lymphoma
o More common in older adults
o Common among persons who are immunosuppressed
 Viruses also implicated as possible cause
 Multi-centric in origin, non-continuous spread to lymph nodes and early to liver, spleen, and bone marrow
 Poorer prognosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Malignant Lymphomas Symptoms

A

 Painless, enlarged lymph nodes
 Low grade fever, night sweats, weight loss, fatigue
 Enlarged liver, spleen

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Malignant Lymphomas Diagnosis

A

 Biopsy lymph node
 CT scan
 Bone marrow aspiration

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Malignant Lymphoma: Treatment

A

• Hodgkin’s Lymphoma
 If localized, radiation therapy alone (Stage I & II)
 Stage IIIA: radiation therapy and combination chemotherapy
 Stage IIIB & IV: combination chemotherapy
• Usually combination of radiation therapy and chemotherapy as multicentric (multiple centers of origin) in nature

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Multiple Myeloma

A

• Malignant disease of plasma cells – abnormal B cells
• Malignant plasma cells produce
 Immune deficiency
 Increased amount of nonfunctional immunoglobulin
o Called the M protein – increases blood viscocity
 Substance that stimulates and enhances angiogenesis
• Malignant plasma cells can infiltrate other tissues

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Multiple Myeloma Symptoms

A

 Bone pain
 Osteoclastic activity increased
o Osteolytic lesions and evidence of osteoporosis on X-ray
o Pathologic fractures
 Hypercalcemia, anemia, leukopenia, thrombocytopenia
 Renal failure (damage due to Bence Jones protein)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Multiple Myeloma Diagnosis

A

 Serum protein electrophoresis
o Elevated monoclonal protein spike
 Bone marrow aspiration
o Sheets of plasma cells present

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Multiple Myeloma Treatment

A

 Chemotherapy: control illness
o Various cheme agents + corticosteroids (Decadron)
 Thalidomide (Thalomid) to prevent angiogenesis (used to be used to treat, but caused deformed limbs if mother took in early pregnancy)
 Biologic agents – alpha-interferon to maintain remission
 Radiation for bone lesions
 Bisphosphonates to diminish osteoclastic activity
 Promote renal function
 Symptom management
o Pain, hypercalcemia, increased blood viscosity
o Prevent, treat infections

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Anemia

A 
•	Reduction in total number of erythrocytes in circulating blood or in the quality or quantity of hemoglobin
	Impaired erythrocyte production
	Acute or chronic blood loss
	Increased erythrocyte destruction
	Combination of the above
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Anemia Morphology

A 
	Morphology
o	Based on MCV, MCH, and MCHC values
o	Size
	Identified by terms that end in “-cytic”
	Macrocytic, microcytic, normocytic
o	Hemoglobin content
	Identified by terms that end in “-chromic”
	Normochromic and hypochromic
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Anemia Physiology Manifestation

A

o Reduced oxygen-carrying capacity
o Heme iron: organ meats good source
o Non-heme irons: Vitamin C helps observe

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Classic Anemia Symptoms

A

Fatigue, dypsnea, weakness, and pallor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Microcytic-Hypochromic Anemia

A

• Iron deficiency anemia
 Most common type of amemia worldwide
 Nutritional iron deficiency
 Metabolic or functional deficiency
 Characterized by RBCs that are abnormally small and contain reduced amounts of hemoglobin
 Related to:
o Disorders of iron metabolism
o Alcoholism
o Progression of iron deficiency causes:
 Brittle, thin, coarsely ridged, and spoon-shaped nails
 A red, sore, and painful tongue

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Macrocytic-Normochromic Anemia

A

• Folate deficiency anemia
 Absorption of folate occurs in the upper small intestine
 Not dependent on any other factor
 Neurologic manifestations generally not seen
 Treatment requires daily oral administration of folate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Normocytic-Normochromic Anemia

A 
•	Hemolytic anemia
	Accelerated destruction of RBCs
	Autoimmune hemolytic anemias
	Immunohemolytic anemia: blood transfusion reaction
	Drug-induced hemolytic anemia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Pernicious Anemia

A

• Lack in intrinsic factor, no B12 absorption
• Signs and symptoms
 Nerve demyelination
 Atrophic glossitis (redness and swelling of tongue, beefy red)
• People at risk usually obese due to surgeries

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Mononucleosis

A

Infection of B lymphocytes
• Epstein Barr virus
• Most infectious two weeks before symptoms start to show
• Ruptured spleen can be caused by this which can cause death
• Diagnosed by monospot test

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

Burkitt-lymphoma

A
  • B-cell, Epstein Barr
  • Most common types of non-Lodgkins lymphoma in children
  • Found in jaw and facial muscles
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

Gas transport

A

 Ventilation of the lungs
 Diffusion of oxygen from the alveoli into the capillary blood
 Perfusion of systemic capillaries with oxygenated blood
 Diffusion of oxygen into systemic capillaries into the cells
 Diffusion of CO2 occurs in reverse order

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

Factors Affecting Alveolar-Capillary Gas Exchange

A
  • Surface area available for diffusion
  • Thickness of the alveolar-capillary membrane
  • Partial pressure of alveolar gases
  • Solubility and molecular weight of the gas
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

Lung compliance

A
  • C=△V/△P

* △V Lung volume can be accomplished with given △P respiratory pressure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

Airway resistance

A
  • Volume of air that moves into and out of the air exchange portion of the lungs
  • Directly related to the pressure difference between the lungs and the atmosphere
  • Inversely related to resistance the air encounters as it moves through the airways
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

Cheyne-Stokes Respirations

A

o Characterized by oscillation of ventilation between apnea and hyperpnea
o Compensate for changing serum partial pressures

41
Q

Kussmaul Respirations

A

o Deep and labored breathing pattern often associated with severe metabolic acidosis, particularly diabetic ketoacidosis (DKA), but also renal failure
o Form of hypertentilation (reduces CO2 in blood due to increased rate or depth of respiration)

42
Q

Signs and Symptoms of Pulmonary Disease

A

• Dyspnea: not breathing properly
 Subjective sensation of uncomfortable breathing
• Orthopnea: difficulty breathing when laying down
• Paroxysmal nocturnal dyspnea (PND): sleeping and then wake up sharply, can be associated with cardiac

43
Q

Mechanisms Involved in Dyspnea

A

• Stimulation of lung receptors
• Increased sensitivity to changes in ventilation perceived through CNS mechanisms
• Reduced ventilatory capacity or breathing reserve
• Stimulation of neural receptors in the muscle fibers of the intercostals and diaphragm and of receptors in the skeletal joints
• Associated conditions
 Primary lung disease
 Heart disease
 Neuromuscular disorders

44
Q

Signs and Symptoms of Pulmonary Disease

A 
•	Hypoventilation
	Hypercapnia
•	Hyperventilation
	Hypocapnia
•	Cough
	Acute cough
	Chronic cough
•	Hemoptysis: coughing up blood
•	Cyanosis
•	Pain: chest pain
•	Clubbing: finger nails, pulmonary obstructive disorders
•	Abnormal sputum: look for color (green, yellow, pink, brown), consistency, thickness, copious amounts of sputum, smell
•	Pulmonary edema: fluid in or around lungs, congestive heart failure (CHF)
45
Q

Hypoxemia

A

• Shortness of breath, increased respiration, changing mental status (esp in elderly), pale or cyanosis
• Results from:
 Inadequate O2 in air
 Disease of respiratory system
 Dysfunction of the neurological system
 Alterations in circulatory function
• Mechanisms
 Hypoventilation
 Impaired diffusion of gases
 Inadequate circulation of blood through the pulmonary capillaries
 Mismatching of ventilation and perfusion

46
Q

Mild Hypoxemia

A 
	Metabolic acidosis
	Increase in heart rate
	Peripheral vasoconstriction
	Diaphoresis
	Increase in blood pressure
	Slight impairment of mental performance
47
Q

Chronic Hypoxemia

A 
	May be insidious in onset and attributed to other causes
o	Compensation masks condition
	Increased ventilation
	Pulmonary vasoconstriction
	Increased production of RBCs
	Cyanosis
48
Q

Hypercapnia

A

• Increased arterial PCO2
• Caused by hyperventilation or mismatching or ventilation and perfusion
• Effects
 Acid-base balance (decreased pH, respiratory acidosis)
 Kidney function
 NS function
 Cardiovascular function

49
Q

Pleural effusion

A

Abnormal collection of fluid in pleural cavity
 Transudate or exudate, purulent (containing pus), chyle (fluid that consists of fat droplets and lymph), or sanguineous (bloody)

50
Q

Spontaneous Pneumothorax

A

 Occurs when air-filled blister on the lung surface ruptures

51
Q

Traumatic Pneumothorax

A

 Caused by penetrating or non-penetrating injuries

 Can be from car accident, incident is involved

52
Q

Tension Pneumothorax

A

 Occurs when the intrapleural pressure exceeds atmospheric pressure
 Build-up of air within pleural space, usually due to a laceration which allows air to escape in pleural space but doesn’t return

53
Q

Characteristics and Symptoms of Pleural Pain

A
  • Abrupt in onset
  • Unilateral, localized to lower and lateral part of the chest
  • May be referred to the shoulder
  • Usually made worse by chest movements
  • Tidal volumes are kept small
  • Breathing becomes more rapid
  • Reflex splinting of the chest may occur
54
Q

Diagnosis of Pleural Effusion

A

 Chest radiographs, chest ultrasound

 Computed tomography (CT)

55
Q

Treatment of Pleural Effusion

A
  • Thoracentesis: inserting needle in lungs to draw out fluid
  • Injection of sclerosing agent (develops scar tissue) into the pleural cavity
  • Open surgical drainage (chest tube, usually used to inflate lungs that collapse)
56
Q

Actelectasis

A

Incomplete expansion of a lung or portion of a lung

57
Q

Causes of Actelectasis

A

 Airway obstruction
 Lung compression such as occurs in pneumothorax or pleural effusion
 Increased recoil of lung due to loss of pulmonary surfactant

58
Q

Causes of Respiratory Failure

A 
•	Impaired ventilation
	Upper airway obstruction
	Weakness of paralysis of respiratory muscles
	Chest wall injury
•	Impaired matching of ventilation and perfusion
•	Impaired diffusion
	Pulmonary edema
	Respiratory distress syndrome
59
Q

Treatment of Respiratory Function

A
  • Respiratory supportive care directed toward maintenance of adequate gas exchange
  • Establishment of an airway
  • Use of bronchodilating drugs
  • Antibiotics for respiratory infections
  • Ensure adequate oxygenation
60
Q

Acute Respiratory Distress Syndrome (ARDS)

A

Damaged alveoli, oxygenation severely impaired
• Injury to pulmonary capillary endothelium
• Inflammation and platelet activation
• Surfactant inactivation
• Atelectasis

61
Q

Causes of ARDS

A
  • Aspiration in gastric contents
  • Major trauma (with or without fat emboli)
  • Sepsis secondary to pulmonary or non-pulmonary infections
  • Acute pancreatitis
  • Hematologic disorders
  • Metabolic events
  • Reactions to drugs and toxins
62
Q

ARDS Manifestations

A 
	Hyperventilation
	Respiratory alkalosis
	Dyspnea and hypoxemia
	Metabolic acidosis
	Hypoventilation
	Respiratory acidosis
	Further hypoxemia
	Hypotension, decreased cardiac output, death
63
Q

ARDS Evaluation and Treatment

A
  • 100% oxygen
  • Keep O2 levels above 90%
  • Physical examination, blood gases, and radiologic examination
  • Supportive therapy with oxygenation and ventilation and prevention of infection
  • Surfactant to improve compliance
64
Q

Chronic obstructive airway disease (COPD)

A

• Expiration is affected
• Progression can be slowed with treatment
• Inflammation and fibrosis of bronchial wall
• Hypertrophy of submucosal glands
• Hypersecretion of mucus (asthmatic patients, chronic bronchitis patients)
• Loss of elastic lung fibers
 Impairs the expiratory flow rate, increases air trapping, and predisposes to airway collapse
• Alveolar tissue
 Decreases the surface area for gas exchange

65
Q

Causes of COPD

A
  • Chronic bronchitis
  • Emphysema
  • Bronchiectasis
  • Cystic fibrosis
66
Q

Types of COPD

A

• Emphysema
 Enlargement of air spaces (beyond terminal bronchioles, loss of recoil, harder and not as quick) and destruction of lung tissue
• Chronic obstructive bronchitis
 Obstruction of small airways

67
Q

Pulmonary Emphysema

A
  • Smoking history
  • Age of onset: 40-50 years
  • Often dramatic barrel chest (1:1 ratio)
  • Weight loss
  • Decreased breath sounds
  • Normal blood gases until late in disease process
  • Slowly debilitating disease
68
Q

Chronic Bronchitis

A
  • Smoking history
  • Age of onset 30-40 years
  • Barrel chest may be present
  • Shortness of breath predominant early symptom
  • Rhonchi often present
  • Sputum frequent early manifestation
  • Often dramatic cyanosis
  • Hypercapnia and hypoxemia may be present
  • Frequent cor pulmonale and polycythemia
  • Numerous life threatening episodes due to acute exacerbations
69
Q

Pulmonary Embolism

A

• Development
 Blood-borne substance lodges in a branch of the pulmonary artery and obstructs the flow

 Thrombus: arising from DVT
 Fat: mobilized from the bone marrow after a fracture or from a tramatized fat depot
 Amniotic fluid: enters the maternal circulation after rupture of the membranes at the time of delivery

70
Q

Asthma

A 
	Environmental
o	Construction (concrete dust)
o	Smoking
o	Pet hair
	Preventable
o	Control whatever triggers asthma attack
	Exercise induced
	Allergen induced 
	Stress Induced
71
Q

Asthma Symptoms

A

Wheezing, coughing throughout the night, difficulty breathing, and excess sputum

72
Q

Pneumonia

A 
	6th leading cause of death
	Nosocomial Infection
	Spread of respiratory droplets
	Hospital/environmental acquired
	Can be caused by bacteria (strep)
	Haemophilis influenza most common cause
73
Q

Tuberculosis

A 
	Caused by mycobacteria (rod-shaped)
	Acid-fast bacillus
	Airborne
	Patients in negative air-pressure rooms
	Droplet precautions
	Causeous necrosis (cheesy-looking granules)
	TB skin tests
o	Pos. needs further testing
o	Chest x-ray
o	3 sputum cultures
74
Q

Hyperthyroidism

A

 Thyrotoxicosis: caused by too much thyroid hormone in body, most common type of hyperthyroidism
o Exopathalmos: bulging of eyes
o Too much T3 and T4 in body
o Cured with iodine
 Graves disease
o Pretibial myxedema
o Most common type of hyperthyroidism
 Hyperthyroidism resulting from nodular thyroid disease
o Goiter: result of iodine deficiency
 Thyrotoxic crisis: immediate care needed, most extreme form of hyperthyroidism

75
Q

Hypothyroidism

A 
•	Primary hypothyroidism
	Subacute thyroiditis
	Autoimmune thyroiditis (Hashimoto disease)
	Painless thyroiditis
	Postpartum thyroiditis
	Myxedema coma: life threatening
•	Congenital hypothyroidism
•	Thyroid carcinoma
•	Overweight, fatigue, thyroid gland can atrophy, constipation, sensitivity to cold, dry skin and nails, constant pain
•	Creatinism	
	44 in or less
	Scamp or no hair
	Umbilical hernia
	Underdeveloped breasts
76
Q

Type 1 Diabetes Mellitus

A
  • Demonstrates pancreatic atrophy and specific loss of beta cells
  • Macrophages, T- and B-lymphocytes, and natural killer cells are present
77
Q

Type 1 Diabetesx Mellitus

A
  • T cells attack and destroy islet cells in pancreas
  • Body can make insulin but body can’t use it
  • Obesity
  • Hypertension
  • Poor wound healings
  • Peripheral neuropathy
  • Amputations
  • Frequent infections
  • Liver and kidney disease
  • End-stage renal disease
  • retinopathy
78
Q

Type 1 DM

A

• Genetic susceptibility
 Glycogen
• Environmental factors
• Immunologically mediated destruction of beta cells by T cells
• Manifestations
 Hyperglycemia, polydipsia, polyuria, polyphagia, weight loss, and fatigue
 Have to have insulin

79
Q

Type 2 DM

A

 Insulin resistance
• Body makes insulin, but doesn’t produce enough for glucose in body
• Usually seen in 35 years +
• Normal should be 70-100
• Orange juice given to help instantly (monosaccharide)
• Milk if no OJ present (dissacharide)
• Glucose given under gum or by IV

80
Q

Acute Complications of DM

A
  • Hypoglycemia
  • Diabetic ketoacidosis
  • Hyperosmolar hyperglycemic nonketotic syndrome (HHNKS)
  • Somogyi effect
  • Dawn phenomenon
81
Q

Diabetic ketoacidosis

A

 Sweet smelling pee
 Fat begins to be broken down
 Carbs aren’t broken down, glucose not used for energy
 Ketones enter bloodstream

82
Q

Hyperosmolar hyperglycemic nonketotic syndrome (HHNKS)

A

 Life threatening
 Enough insulin produced to not get NKA
 Not enough insulin produced to not prevent hyperglycemia
 High blood sugarm but body still making enough insulin
 Ketones aren’t spilled into blood

83
Q

Somogyi effect

A

Blood glucose drops in sleep, Hormones increase blood sugar too much

84
Q

Dawn phenomenon

A

Higher blood sugar than anticipated when waking up

85
Q

Chronic Complications of DM

A 
•	Hyperglycemia and nonenzymatic glycosylation
•	Hyperglycemia and the polyol pathway
	Protein kinase C
•	Microvascular disease
	Retinopathy
	Diabetic nephropathy
•	Macrovascular disease
	Coronary artery disease
	Stroke 
	Peripheral arterial disease
•	Diabetic neuropathies
•	Infection
86
Q

Disseminated Intravascular Coagulation (DIC)

A

• Complex, acquired disorder in which clotting and hemorrhage simultaneously occur
• Result of increased protease activity in the blood caused by unregulated release of thrombin with subsequent fibrin formation and accelerated fibrinolysis
• Endothelial damage is the primary initiator of DIC
• By activating fibrinolytic system (plasmin), patient’s fibrin degradation product (FDP) and D-dimer levels will increase
• Because of the patient’s clinical state, the disorder has a high mortality rate
• Treatment is to remove the stimulus and maintain hemodynamic status
• Clinical signs and symptoms demonstrate wide variability
 Bleeding from venipuncture sites
 Bleeding from arterial lines
 Purpura, petechiae, and hemotomas
 Symmetric cyanosis of the fingers and toes

87
Q

Vitamin K deficiency

Alteration of Coagulation

A

Necessary for synthesis and regulation of prothrombin, the prothrombin factors (II, VII, XI, X) and proteins C and S (anticoagulants)

88
Q

Liver disease

A

 Causes a broad range of hemostasis disorders

o Defects in coagulation, fibrinolysis, and platelet number and function

89
Q

Thrombocytopenia

A

Platelet count <150,000/mm3

90
Q

Hemorrhage from minor trauma

A

<50,000/mm3

91
Q

Spontaneous bleeding

A

<15,000/mm3

92
Q

Severe bleeding

A

<10,000/mm3

93
Q

Sickle Cell Anemia

A

Mutation in beta chains of HbG

When HbG deoxygenated, beta chains link together forming long protein rods that make the cell sickle

94
Q

Problems caused by Sickle Cell

A

Blocked capillaries, causing acute pain, infarctions cause chronic damage to liver, spleen, heart, kidneys, eyes and bones
Pulmonary infarction > acute chest syndrome
Cerebral infarction > stroke
Sickled cells more likely to be destroyed

95
Q

Ventilation

A

the movement of air between the atmosphere and the respiratory portion of the lungs

96
Q

Inspiration

A

air is drawn into the lungs as the respiratory muscles expand the chest cavity

97
Q

Expiration

A

air moves out of the lungs as the chest muscles expand the chest cavity becomes smaller

98
Q

Perfusion

A

the flow of blood through the lungs

99
Q

Diffusion

A

transfer of gases between air-filled spaces in the lungs and the blood

Pathophysiology (2 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions