Exam 3 Flashcards
1
Q
What is Poikilocytosis?
A
Red blood cells have abnormal shapes
2
Q
What is Anisocytosis?
A
Red blood cells (RBCs) abnormal sizes
3
Q
What is anemia?
A
A reduction in the total number of erythrocytes in the circulating blood or a decrease in the quality or quantity of hemoglobin
4
Q
What are the common causes of anemia? (Think mechanisms. Like, what does a B12 deficiency do that would cause anemia?)
A
- Impaired erythrocyte production
- Blood loss (acute or chronic)
- Increased erythrocyte destruction
- Combination of these factors
5
Q
What is Megaloblastic Anemia (MA)?
A
A type of anemia that causes red blood cells to be abnormally large and not fully developed due to impaired DNA synthesis
6
Q
What are megaloblasts?
A
Large red blood cell precursors found in the bone marrow due to megaloblastic anemia
7
Q
What is an example of Megaloblastic Anemia?
A
Pernicious Anemia (PA)
8
Q
What is the main disorder in Pernicious Anemia?
A
An absence of intrinsic factor (IF)
9
Q
What is intrinsic factor (IF)?
A
A glycoprotein produced in the stomach that binds to vitamin B12 for absorption in the intestines
10
Q
What can vitamin B12 deficiency lead to? Think cellular level. Disorders of what two systems?
A
- Abnormal red blood cell precursor cells (megaloblasts)
- Enlarged RBCs in circulation (macrocytes)
- Hematologic and neuropsychiatric disorders
11
Q
What characterizes Microcytic-Hypochromic Anemias?
A
Abnormally small erythrocytes that contain unusually reduced amounts of hemoglobin
12
Q
What is the most common nutritional disorder of Microcytic-Hypochromic Anemia?
A
Iron deficiency anemia (IDA)
13
Q
What can cause Iron Deficiency Anemia (IDA)?
A
- Inadequate dietary intake
- Excessive blood loss
14
Q
What is a common symptom of Iron Deficiency Anemia (IDA)?
A
Fatigue
15
Q
What is Normocytic-Normochromic Anemia?
A
Anemia characterized by normal-sized red blood cells with normal hemoglobin content
16
Q
What is Aplastic Anemia?
A
A critical condition characterized by pancytopenia due to failure or suppression of bone marrow
17
Q
What causes Aplastic Anemia?
A
- Autoimmune disease against hematopoiesis
- Exposure to chemical agents
- Idiopathic causes
18
Q
What is Disseminated Intravascular Coagulation (DIC)?
A
An acquired clinical syndrome characterized by widespread activation of coagulation, leading to fibrin clots
19
Q
What is the most common condition associated with DIC?
A
Sepsis
20
Q
True or False: Individuals with DIC are at risk for hemorrhage.
A
True
21
Q
What distinguishes Hodgkin Lymphoma (HL) from Non-Hodgkin Lymphoma (NHL)?
A
HL is characterized by progression from one group of lymph nodes to another and the presence of Reed-Sternberg (HRS) cells
22
Q
What is the hallmark of Hodgkin Lymphoma (HL)?
A
Presence of Reed-Sternberg (HRS) cells
23
Q
What is Hereditary Hemochromatosis (HH)?
A
An inherited disorder causing iron accumulation in tissues and organs
24
Q
How is Hereditary Hemochromatosis inherited?
A
In an autosomal recessive pattern
25
What can happen due to iron accumulation in Hereditary Hemochromatosis? Don’t forget: what is the relationship to diabetes??
* Disruption of organ function
* Injury to pancreatic B-islet cells leading to diabetes
26
Fill in the blank: The actual prevalence of vitamin B12 deficiency may be higher than statistics indicate due to the use of _______ and the _____ of the U.S. population.
gastric acid–blocking agents
aging
27
A chronic, relapsing, proliferative, immune mediated inflammatory disorder involving the skin, scalp, and nails.
Psoriasis
28
What are common comorbidities associated with psoriasis onset later in life?
* Obesity
* Smoking
* Hypertension
* Diabetes
29
What cells are involved in the inflammatory cascade of psoriasis? (6 types)
* Macrophages
* Fibroblasts
* Dendritic cells
* Natural killer cells
* T-helper cells
* Regulatory T cells
30
What changes occur in the epidermis and dermis in psoriasis? (3)
Both are thickened due to cellular hyperproliferation, altered keratinocyte differentiation, and expanded dermal vasculature.
31
What is the normal epidermal shedding time compared to that in psoriasis?
Normal is 14 to 20 days; in psoriasis, it escalates to 3 to 4 days.
32
What causes Lyme disease?
It is caused by the spirochete Borreliella burgdorferi.
33
How is Lyme disease transmitted?
By the bite of the Ixodes tick.
34
What is erythema migrans?
A bull's-eye rash associated with Lyme disease.
35
True or False: There is a vaccine for Lyme disease.
False
36
What are the two types of herpes simplex virus (HSV) and their common transmission routes?
* HSV-1: Spread through oral secretions
* HSV-2: Genital infections, spread by skin-to-skin mucous membrane contact
37
What is a significant risk factor for HSV infection?
Immunosuppression or sexual contact with infected individuals.
38
What happens during vertical transmission of HSV-2?
It is associated with significant neonatal neurologic morbidity and mortality.
39
How does the herpes simplex virus maintain lifelong latency?
By inhibiting apoptosis of target cells.
40
What can trigger reactivation of herpes simplex virus?
* Ultraviolet light
* Skin irritation
* Fever
* Fatigue
* Stress
41
What are nevi?
Benign pigmented or nonpigmented lesions.
42
Melanocytic nevi can be congenital or ________.
Acquired
43
What is the ABCDE rule used for?
To evaluate suspicious pigmented nevi.
44
What does 'A' in the ABCDE rule stand for?
Asymmetry
45
What does 'B' in the ABCDE rule stand for?
Border irregularity
46
What does 'C' in the ABCDE rule stand for?
Color variation
47
What does 'D' in the ABCDE rule stand for?
Diameter larger than 6 mm
48
What does 'E' in the ABCDE rule stand for?
Elevation or Evolving
49
What is cutaneous melanoma?
A malignant tumor of the skin originating from the transformation of melanocytes.
50
Where do melanocytes arise from?
Neural crest tissue.
51
What is basal cell carcinoma (BCC) primarily caused by?
UV radiation exposure.
52
What is a common appearance of basal cell carcinoma?
A nodule greater than 5 mm that is pearly or ivory and slightly elevated.
53
True or False: Metastatic spread is common in basal cell carcinoma.
False
54
What is seborrheic keratosis?
A benign proliferation of cutaneous basal cells producing flat or slightly elevated lesions.
55
At what age do seborrheic keratosis lesions typically appear?
Usually in people over the age of 50, but can appear in young adults.
56
What are effective treatments for seborrheic keratosis?
* Cryotherapy with liquid nitrogen
* Shave excisions
* Laser therapy
57
Where does acne vulgaris form?
Acne develops at distinctive pilosebaceous units known as sebaceous follicles.
58
What hormones increase during puberty that affect acne development?
Androgens such as dehydroepiandrosterone sulfate and testosterone.
59
How do androgens influence sebaceous glands?
They increase the size and productivity of the sebaceous glands, promoting comedome formation.
60
What bacteria are involved in the development of acne vulgaris?
Cutibacterium acnes (C. acnes).
61
What happens to C. acnes strains during acne development?
They shift from being symbiotic to a pathogenic strain.
62
What triggers inflammatory mediators in acne vulgaris?
Ruptured comedones.
63
What is atopic dermatitis also known as?
Atopic eczema.
64
What age range is most commonly affected by atopic dermatitis?
Onset is usually from 2 to 6 months of age.
65
What are common comorbidities associated with atopic dermatitis?
* Asthma
* Allergic rhinitis
* Food allergies
66
What is the role of immunoglobulin E (IgE) in atopic dermatitis?
Increased serum levels of IgE are observed.
67
What is the most common bacterial skin infection in children aged 2 to 5?
Impetigo.
68
What bacteria primarily cause impetigo?
* Staphylococcus aureus
* Streptococcus pyogenes (less common)
69
How is impetigo transmitted?
By both direct and indirect contact.
70
What do staphylococci produce that affects the skin barrier in impetigo?
Bacterial toxins known as exfoliative toxins (ETs).
71
What virus causes molluscum contagiosum?
A pox virus.
72
How is molluscum contagiosum spread?
* Person-to-person direct contact
* Auto inoculation
* Contaminated fomites
73
What are the two primary mechanisms that can lead to significantly elevated or depressed hormone levels?
1. Inappropriate amounts of hormone delivered to the target cell
2. Inappropriate responses by the target cell
74
What can cause inappropriate amounts of hormone in the body?
Disorders of endocrine glands, failure of feedback systems, dysfunctional or ectopically produced hormones, defects in hormone delivery
75
What is the role of antidiuretic hormone (ADH)?
ADH is released when there is not enough fluid in the body, helping to retain water
76
What condition results from insufficient levels of ADH?
Diabetes insipidus
77
What are the symptoms of diabetes insipidus?
Polyuria and polydipsia due to volume depletion
78
What is neurogenic diabetes insipidus associated with?
Traumatic brain injuries
79
What characterizes the syndrome of inappropriate antidiuretic hormone (SIADH) secretion?
High levels of ADH in the absence of normal physiological stimuli
80
What are some conditions associated with SIADH?
Ectopic secretion by tumors, pulmonary disorders, central nervous system disorders
81
What is the result of dilutional hyponatremia in SIADH?
Hypervolemia, high urinary sodium concentration, and weight gain
82
What functions are associated with the thyroid gland?
Metabolism, growth, and development
83
How does thyroid hormone use a negative feedback loop?
Low T3 and T4 levels stimulate TRH release, leading to TSH production, which raises thyroid hormone levels
84
What do high TSH levels indicate?
Hypothyroidism
85
What do low TSH levels indicate?
Hyperthyroidism
86
What are some symptoms of hypothyroidism?
Constipation, bradycardia, dyspnea, lethargy
87
What is Graves Disease?
A form of hyperthyroidism due to stimulation of the thyroid by autoantibodies against the TSH receptor
88
What characterizes diabetes mellitus type I?
Pancreatic dysfunction and beta cell destruction leading to absolute insulin deficiency
89
What is the most common form of diabetes type I?
Immune-mediated diabetes
90
What characterizes diabetes mellitus type II?
Defects in pancreatic insulin secretion and insulin resistance, leading to persistent hyperglycemia
91
What are some risk factors for diabetes type II?
Obesity, poor diet, lack of regular exercise
92
What does insulin resistance refer to?
Suboptimal response of insulin-sensitive tissues to insulin
93
What is glucagon-like peptide 1 (GLP-1)?
An incretin that should decrease blood glucose levels
94
How does obesity contribute to insulin resistance?
Increased adipokines, free fatty acids, inflammation, and mitochondrial dysfunction
95
What are adipokines?
Cytokines produced by adipose tissue
96
What effect does increased leptin and decreased adiponectin have?
It results in inflammation and decreased insulin sensitivity
97
What leads to decreased tissue responses to insulin in obesity?
Increased free fatty acids and intracellular deposits of triglycerides and cholesterol
98
Obesity is one of the most important contributors to insulin resistance and diabetes. What are the four changes in cells due to obesity contribution to insulin resistance?
1. Increased adipokines: increased leptin (leptin resistance) and decreased adiponectin. These two things cause inflammation and decreased insulin sensitivity.
2. Increase free fatty acids: intracellular deposits of triglycerides and cholesterol lead to decreased tissue responses to insulin
3. Inflammation: adipocyte-associated pro-inflammatory macrophages and inflammatory cytokines released from adipocytes induce insulin resistance, and are cytotoxic to beta cells.
4. Mitochondrial dysfunction: decreased insulin-induced mitochondrial activity leads to insulin resistance.
99
What is the impact of mitochondrial dysfunction on insulin resistance?
Decreased insulin-induced mitochondrial activity
100
What is diabetes ketoacidosis (DKA)?
A serious complication related to a deficiency of insulin and increased levels of insulin counterregulatory hormones.
## Footnote
DKA is characterized by hyperglycemia, acidosis, and ketonuria.
101
What are the key characteristics of DKA?
Hyperglycemia, acidosis, ketonuria.
## Footnote
DKA is more common in type 1 diabetes due to greater insulin deficiency.
102
What causes the production of ketone bodies in DKA?
Insulin deficiency enhances lipolysis, increasing fatty acids delivered to the liver, leading to increased glyconeogenesis and ketone body production.
## Footnote
Key ketone bodies include acetoacetate, hydroxybutyrate, and acetone.
103
What are the symptoms of DKA?
Kussmaul respirations, postural dizziness, CNS depression, ketonuria, anorexia, nausea, vomiting, abdominal pain, thirst, polyuria.
## Footnote
Kussmaul respirations are hyperventilation attempts to compensate for acidosis.
104
How is DKA managed?
Combination of fluids, insulin, and electrolyte replacement.
105
What is hyperosmolar hyperglycemic nonketotic syndrome (HHNKS)? It is precipitated by what 4 things?
A life-threatening emergency most often precipitated by infections, medications, nonadherence to diabetes treatment, or coexisting disease.
## Footnote
HHNKS is more common in type 2 diabetes.
106
What characterizes diabetic microvascular complications?
Disease in capillaries leading to retinopathy, kidney failure, and neuropathies.
## Footnote
Thickening of the capillary basement membrane and endothelial cell hyperplasia contribute to decreased tissue perfusion.
107
What are the leading conditions caused by diabetic microvascular complications?
* Retinopathy (leading to blindness)
* Kidney disease (leading to end-stage kidney failure)
* Diabetic neuropathies.
108
What is macrovascular disease associated with diabetes?
Lesions in medium and large-sized arteries increasing morbidity and mortality, risk for accelerated atherosclerosis, myocardial infarction, and stroke.
109
Why do individuals with diabetes have higher mortality during myocardial infarctions?
They are often asymptomatic due to sensory and autonomic neuropathy.
110
What is the significance of monitoring glycosylated hemoglobin (Hb A1c) in diabetes?
It determines glucose control over 3 to 4 months.
111
What characterizes Addison disease?
Inadequate corticosteroid and mineralocorticoid synthesis and elevated serum ACTH levels.
112
Hypocortisolism and hypoaldosteronism, leading to hyperkalemia and hypovolemia are all seen in what disease?
Addison disease
113
What is Cushing syndrome?
A general term for ALL clinical manifestations related to excessive exposure to cortisol.
114
What are common signs, including electrolyte deficiencies, of Cushing syndrome?
* Hypernatremia
* Hyperglycemia
* Hypokalemia
* Weight gain (truncal obesity, moon face, buffalo hump).
115
What causes glucose intolerance in Cushing syndrome?
Cortisol-induced insulin resistance and increased gluconeogenesis and glycogen storage by the liver.
116
What is the effect of cortisol on muscle tissue?
Causes protein wasting and muscle weakness, especially in extremities.
117
What are the integumentary effects of Cushing syndrome?
Loss of collagen leads to thin, weakened tissues, purple striae, and easy bruising.
118
What is Cushing disease?
Refers to clinical manifestations from chronic exposure to excess endogenous cortisol, more common in women.
119
What does Cushing disease specifically refer to?
Excess endogenous secretion of ACTH (corticotropin).
120
What is short-term starvation?
Short-term starvation consists of several days of total dietary abstinence or deprivation.
121
What happens in the body 4 to 6 hours after the last meal?
The body is in a well-fed state and its energy requirements are supplied by glucose from recently ingested carbohydrates.
122
What process occurs when glycogen in the liver is converted to glucose?
Glycogenolysis.
123
What is long-term starvation?
Long-term starvation begins after several days of dietary abstinence and eventually causes death from proteolysis.
124
Persistent restriction of energy intake leading to significantly low body weight, disturbance in body weight or shape experience, undue influence of body shape and weight on self-evaluation.
Anorexia Nervosa
125
What is a key feature of Bulimia Nervosa?
Recurrent episodes of binge eating with inappropriate compensatory behavior to prevent weight gain.
126
How often do binge eating and inappropriate compensatory behaviors occur in Bulimia Nervosa?
At least once a week for 3 months.
127
What distinguishes Binge Eating Disorder from Bulimia Nervosa?
Binge Eating Disorder is not associated with recurrent use of inappropriate compensatory behaviors.
128
List three characteristics of binge eating episodes.
* Eating much more rapidly than normal.
* Eating until feeling uncomfortably full.
* Eating large amounts of food when not feeling physically hungry.
129
A decrease in appetite or food intake in older adults, occurring even in illness-free individuals.
Anorexia of aging
130
What are some age-related changes contributing to Anorexia of aging?
* Reduced energy needs
* Waning hunger
* Diminished senses of smell and taste
* Decreased production of saliva
* Altered gastrointestinal satiety control mechanisms.
131
What are risk factors for Anorexia of aging?
* Functional impairments
* Medical and psychiatric conditions
* Loneliness and grief
* Medications, including polypharmacy
* Social isolation.
132
What are the consequences of Anorexia of aging?
* Malnutrition
* Physical frailty
* Mitochondrial dysfunction
* Reduced regenerative capacity
* Increased oxidative stress.
133
What role does exercise play in treating elderly individuals with Anorexia?
Exercise improves appetite and oral intake, elevates mood, and builds muscle and strength.
134
What are the nonmodifiable risk factors for Coronary Artery Disease?
* Advanced age
* Male gender or women after menopause
* Family history.
135
List modifiable risks for Coronary Artery Disease.
* Dyslipidemia
* Hypertension
* Cigarette smoking
* Diabetes and insulin resistance
* Obesity
* Sedentary lifestyle
* Atherogenic diet.
136
What does an increased serum concentration of LDL indicate?
An indicator of coronary risk.
137
What does HDL cholesterol do?
Responsible for 'reverse cholesterol transport,' returning excess cholesterol from tissues to the liver.
138
What is stable angina?
Predictable chest pain relieved with usual interventions such as nitroglycerin or resting.
139
What distinguishes unstable angina from stable angina?
Unstable angina pain is worse and not relieved by usual interventions.
140
What triggers Vasospastic (Prinzmetal) angina? (5)
* Vasospasm of coronary arteries
* Hyperventilation
* Mental stress
* Smoking
* Alcohol use.
141
How is Vasospastic angina diagnosed?
By matching clinical manifestations with documented transient ischemic changes on ECG.
142
What are the characteristics of Acute Coronary Syndrome (ACS)?
Unstable angina is considered under non-ST elevation MI (NSTEMI) and indicates myocardial damage.
143
What determines the size and character of an NSTEMI?
The duration of ischemia.
144
What happens if the thrombus breaks up before complete distal tissue necrosis in NSTEMI?
The infarction will involve only the myocardium directly beneath the endocardium (subendocardial MI).
145
What does STEMI stand for?
ST elevation myocardial infarction
146
What is the primary cause of STEMI?
Plaque buildup and rupture obstructing flow in a coronary artery
147
What is a transmural MI?
Infarction extending from endocardium to epicardium
148
What ECG changes are associated with transmural infarction?
Marked elevations in ST segments
149
What hormone is secreted after a myocardial infarction in response to hemodynamic changes?
Angiotensin II
150
What is the most important effect of Angiotensin II after a myocardial infarction?
Increased peripheral vasoconstriction
151
What condition can result from rapid accumulation of fluid in the pericardial sac?
Cardiac tamponade
152
Define heart failure (HF).
Inability of the heart to generate adequate cardiac output, leading to inadequate tissue perfusion or increased diastolic filling pressure
153
What is heart failure with preserved ejection fraction (HFpEF)?
Diastolic heart failure with decreased compliance of the left ventricle
154
What is heart failure with reduced ejection fraction (HFrEF)?
Systolic heart failure with an ejection fraction of <40%
155
What is preload?
The load on the heart created by the volume of blood received into the left ventricle from the left atrium
156
What is afterload?
The resistance the heart encounters when ejecting blood to the rest of the body
157
What does increased afterload do to stroke volume?
Reduces stroke volume
158
What is contractility?
The strength of the heart muscle's contraction
159
What is the role of catecholamines in heart failure?
Compensates for decreased cardiac output by increasing heart rate and peripheral vascular resistance
160
What is the Renin-Angiotensin-Aldosterone System (RAAS)?
A system activated when blood pressure is low, causing increased preload and afterload
161
What substances are included in the RAAS?
* Renin
* Angiotensin II
* Aldosterone
162
What does Angiotensin II do?
Increases peripheral vascular resistance and blood pressure
163
What effect does aldosterone have in the RAAS?
Causes salt and water retention
164
True or False: Heart failure symptoms are different regardless of ejection fraction.
False
165
What happens to cardiac output and pressure in the carotid sinus when ADH is released?
Cardiac output decreases, reducing pressure in the carotid sinus and renal afferent arteriole
## Footnote
This is perceived by the body as volume depletion.
166
What are the effects of Antidiuretic Hormone (ADH) on the body?
Causes peripheral vasoconstriction (AFTERLOAD) and renal fluid retention (PRELOAD)
## Footnote
ADH helps the body retain water and maintain blood pressure.
167
What role do natriuretic peptides play in heart failure?
Counteract neurohumoral processes by improving salt and water excretion
## Footnote
ANPs and BNPs may have protective effects but are inadequate in heart failure.
168
What is the function of B-type natriuretic peptides (BNPs)?
Produced in response to pressure and volume overload; inhibits myocardial fibrosis and hypertrophy
## Footnote
Enhances diastolic function and helps monitor heart failure exacerbation.
169
What is a common complication of congenital heart defects in children?
Heart failure
## Footnote
The etiology varies with age, with newborns often experiencing HF from pulmonary overcirculation.
170
What are common causes of heart failure in older children?
* Viral myocarditis
* Rheumatic heart disease
* Autoimmune disorders
* Anemia
* Kawasaki disease
* Hypothyroidism
## Footnote
Right ventricular failure is rare in children.
171
What is hypertension often referred to as?
The 'silent killer'
## Footnote
Hypertension is often asymptomatic and a major risk factor for heart disease and stroke.
172
What are the first-line treatments for hypertension?
Lifestyle changes
## Footnote
These may include diet, exercise, and smoking cessation.
173
What are some mechanisms involved in the pathophysiology of hypertension?
* Impaired renal pressure natriuresis
* Excessive activation of the sympathetic nervous system
* Increased systemic vascular resistance
## Footnote
These mechanisms contribute to elevated blood pressure.
174
What can impaired renal pressure natriuresis lead to?
Increased sodium and water retention, raising blood volume and blood pressure
## Footnote
This creates a vicious cycle in hypertension.
175
What complications can arise from hypertension regarding the kidneys?
Tissue ischemia and inflammation leading to glomeruli and tubule dysfunction
## Footnote
This can result in microalbuminuria.
176
How does hypertension affect the eyes?
Causes retinopathy by increasing retinal arterial pressure
## Footnote
This damages the microvasculature in the eyes.
177
What is the effect of sustained hypertension on blood vessels?
Accelerates atherosclerosis by damaging blood vessel walls
## Footnote
This leads to plaque formation and narrowed arteries.
178
What are the potential consequences of plaque buildup in arteries due to hypertension?
* Diminished blood flow
* Reduced delivery of nutrients and oxygen
## Footnote
This can significantly impact organs such as the heart, brain, and lower limbs.
179
What is mitral stenosis?
It impairs the flow of blood from the left atrium to the left ventricle.
## Footnote
Outcomes include pulmonary hypertension, edema, and right ventricular failure if untreated.
180
What are the consequences of untreated chronic mitral stenosis?
Pulmonary hypertension, edema, and right ventricular failure.
## Footnote
These outcomes arise from elevated atrial pressure and incomplete emptying of the left atrium.
181
What is mitral regurgitation?
It permits backflow of blood from the left ventricle into the left atrium during ventricular systole.
## Footnote
It can lead to impaired left ventricular function and pulmonary hypertension.
182
What conditions are associated with mitral regurgitation?
Connective tissue disorders such as Marfan syndrome.
## Footnote
As mitral regurgitation progresses, increased atrial pressure can lead to right ventricular failure.
183
What happens in aortic stenosis?
The orifice of the valve narrows, causing resistance to blood flow from the left ventricle into the aorta.
## Footnote
This leads to increased pressure within the left ventricle.
184
What is a consequence of left ventricular hypertrophy due to aortic stenosis?
Gradual decline in left ventricular function with decreased cardiac output.
## Footnote
This can lead to serious complications such as heart failure and myocardial ischemia.
185
What is peripheral artery disease (PAD)?
Atherosclerotic disease of arteries that perfuse the limbs, especially the lower extremities.
## Footnote
It can result in intermittent claudication due to increasing obstruction to arterial blood flow.
186
What are varicose veins?
Superficial veins in which blood has pooled.
## Footnote
They can be caused by trauma or gradual venous distention.
187
What is chronic venous insufficiency (CVI)?
Sustained inadequate venous return.
## Footnote
Signs include edema of the lower extremities and hyperpigmentation of the skin.
188
What is aortic coarctation?
A narrowing of part of the aorta, making it hard for blood to pass through.
## Footnote
It can lead to increased upper extremity blood pressure and poor perfusion of tissues.
189
What are common presentations of aortic coarctation in neonates?
Left ventricular dysfunction and shock from increased afterload.
## Footnote
Physical findings include upper extremity hypertension and signs of poor perfusion.
190
What is Kawasaki disease (KD)?
An acute systemic vasculitis that may result in myocarditis and coronary artery aneurysms.
## Footnote
KD is a leading cause of acquired heart disease among children.
191
What are the immune responses involved in Kawasaki disease?
Release of inflammatory cytokines, increased serum antibodies, and infiltration of vessel walls by immune cells.
## Footnote
This can lead to acute myocarditis and necrotizing arteritis.
192
True or False: Kawasaki disease has a known etiology.
False.
## Footnote
The etiology remains unknown, with theories focusing on abnormal immune responses.
