patho final study guide (1)
Hematopoiesis
- Distributive means vessel issue
Clinical Manifestations of PCOS
- Prolonged menstrual periods
- Hirsutism (facial hair)
- Acne
- Male pattern baldness
- Acanthosis nigricans (darkened discoloration of skin)
Pathophysiology of Endometriosis
- Endometrial tissue is located outside the uterus
- Can result in:
- Pelvic adhesions
- Distortion of pelvic structures
- Dysmenorrhea
Etiology/Causative Agent of PID
- Result of sexually transmitted infection of the reproductive tract
- Chlamydia trachomatis
- Neisseria gonorrhoeae
- Microorganisms spread:
- Into the cervix
- Uterus
- Uterine tubes
- Ovaries
- Into the peritoneal cavity
Causes of Stress Incontinence
- Childbirth
- Pregnancy
- Obesity
- Aging
- Pelvic surgeries (prostatectomy)
Clinical Manifestations of Addison’s Disease
- Low blood sugar
- Weakness
- Fatigue
- Anorexia
- Nausea, vomiting
- Weight loss
- Dehydration
- Hyponatremia
- Hyperkalemia
- Hypotension
Clinical Manifestations of Diabetes Mellitus
Type 1
- Severe hyperglycemia and hyperketonemia
- Polydipsia (excessive thirst)
- Polyuria (excessive urination)
- Polyphagia (excessive hunger)
Type 2
- Related to long-term complications:
- Visual changes
- Changes in kidney function
- Coronary artery disease
- Recurrent infections
Clinical Manifestations of Grave’s Hyperthyroidism
- Enlargement of thyroid gland
- Excessive metabolic rate of the body
- Symptoms:
- Weight loss
- Agitation
- Restlessness
- Sweating
- Heat intolerance
- Diarrhea
- Tachycardia
- Heart palpitations
- Tremors
- Fine hair
- Oily skin
- Irregular menstrual cycle
- Goiter from follicular epithelial cell hyperplasia
- Exophthalmos: protrusion of the eyeball
Electrolyte Imbalance of Patients with SIADH
- Hyponatremia (serum sodium < 135)
- Hypotonicity (plasma osmolality < 280)
- Decreased urine volume
- Highly concentrated urine with high sodium content
- Absence of renal, adrenal, or thyroid abnormalities
Pathophysiology of DKA
- Lack of insulin causes mobilization of fatty acids for energy
- Increased production of ketones
- Kidneys unable to excrete ketones; cells cannot use byproducts
- Ketones accumulate in blood
Pathophysiology of Cushing’s Syndrome
- Hypersecretion of adrenal cortex hormones
- Mainly increased cortisol
- Glucocorticoids contribute to:
- Metabolic function
- Inflammatory/immune response
- Stress response
- Mnemonic: Remember CUSHing’s - there’s a CUSHION of steroids
Pathophysiology of DM1
- Autoimmune destruction
- Multifactorial etiology involving genetic susceptibility and environmental triggers (viruses like mumps and rubella)
- Cell-mediated immune mechanisms with cytotoxic T lymphocytes destroy pancreatic beta cells
- Antibodies against glutamic acid decarboxylase (GAD) enzyme within beta cells
- Chronic inflammatory response contributes to further destruction
- Insulin Deficiency
- Clinical manifestations occur when 80-90% of beta cells are destroyed
- Results in absolute insulin deficiency
- Also affects alpha cell function, causing increased glucagon levels
- Glucagon suppresses insulin production, worsening the condition
- Metabolic Consequences
- Hyperglycemia from glucose accumulation without adequate insulin for cellular uptake
- Hyperketonemia from unregulated fat mobilization
- Fat oxidation produces ketone bodies, leading to metabolic ketoacidosis
- Body utilizes fat stores and protein for energy (cellular starvation)
Possible Causes of Diabetes Insipidus (DI)
- Insufficient production of ADH by hypothalamus or ineffective secretion by posterior pituitary
- Inadequate kidney response to ADH (nephrogenic DI)
- Ingestion of large volumes of fluids/decreased ADH levels; sometimes due to psychiatric disturbances
Lab Test for Glucose Over the Past 3 Months
- A1c: Shows amount of hemoglobin proteins in red blood cells that are coated with sugar
Clinical Manifestations of BPH
- Related to urethral obstruction from enlarged prostate, which impedes urine flow
- Symptoms:
- Urinary frequency
- Dribbling
- Hesitancy
- Incontinence
- Urgency
- Retention
Pathophysiology of Peptic Ulcer Disease
- Infection by H. pylori and chronic NSAIDs usage
- H. pylori damages protective mucus lining of stomach and duodenum
- NSAIDs produce prostaglandins that cause stomach acid erosion
- Alcohol use and smoking can contribute
Example of Passive Immunity
- IgA provides passive immunity from mother to newborn through breast milk, ensuring essential immune defense prior to adequate infant immune response development
Differentiate RA vs OA
Osteoarthritis
- Overview: Progressive breakdown and loss of cartilage in joints due to wear and tear
- Degenerative disease affecting mostly weight-bearing joints
- Risk Factors:
- Old age
- Female
- Obesity
- Repetitive joint stress
- Symptoms:
- Morning stiffness lasting less than 30 minutes
- Hard and bony joints
- No inflammation present
- Nodes can be Bouchard’s or Heberden
Rheumatoid Arthritis
- Overview: Body's immune system attacks joints causing inflammation (autoimmune disease); systemic effects observed
- Risk Factors:
- Age 20-50
- Female
- Family history
- Smoking
- Symptoms:
- Morning stiffness lasting greater than 30 minutes
- Warm, soft, and swollen joints
- Symmetrical and systemic effects
- Nodes can be swan-neck, boutonniere, ulnar drift
ABCDE of Skin Cancer
- A - Asymmetry: A mole that is irregularly shaped
- B - Border: A mole with jagged edges without clear definition
- C - Color: A growth that is multicolored or changes color
- D - Diameter: A sudden increase in mole size, especially one greater than 6mm
- E - Elevation: A flat mole that becomes elevated
Primary Immunodeficiency
- Group of inherited genetic disorders affecting normal immune system development or function
- Present at birth leading to infections and potential autoimmune diseases
Examples of Active Immunity
- Development of antibodies in response to an antigen from having a specific disease or vaccine
Examples of Type 2 Hypersensitivity
- Antibody-mediated reactions such as blood transfusion, Graves’ disease, and hemolytic disease
- When antibodies bind to antigens, cells are lysed and destroyed resulting in decreased red blood cells, decreased platelets, and leukopenia
- Mediated by IgG or IgM
Possible Causes of Hypovolemia (Fluid Volume Deficit)
- Causes:
- GI losses (vomiting, diarrhea)
- Renal loss (diuretics, diabetes)
- Third spacing (ascites, edema)
- Swelling
- Pathophysiology:
- Reduced intravascular volume leads to decreased venous return
- Results in reduced cardiac output, hypotension, and poor organ perfusion
- Clinical Signs:
- Tachycardia
- Hypotension
- Orthostatic changes
- Decreased urine output
- Altered mental status
Intracellular Fluid
- Found inside cells, rich in potassium and proteins
- Found outside cells, high in sodium and chloride
Differentiate Diffusion vs Osmosis
Simple Diffusion
- Works for small, lipid-soluble molecules (e.g., O2, CO2) passed through the lipid bilayer
- Movement follows concentration gradients until equilibrium is reached; particle size and membrane pore size affect rate
Facilitated Diffusion
- Important for larger molecules (e.g., glucose) or ions that cannot cross on their own
- Transport proteins act as selective channels or carriers
- Types:
- Leak Channels: Open without stimulation
- Gated Channels: Open and close in response to stimuli
- Voltage-gated: Stimulated by change in membrane potential
- Ligand-gated: Stimulated by receptor-ligand binding
- Mechanically gated: Stimulated by vibration, stretching and pressure
Osmosis
- Water movement across a semipermeable membrane along concentration gradient; osmotic pressure is crucial for maintaining cell volume and turgor pressure
Active Transport: Electrolyte and Fluid Movement
- Energy-requiring process moving substances against their concentration gradient
- Sodium Potassium Pump: Uses ATP to pump sodium out and potassium into cells, both against gradients
- Types:
- Primary Active Transport: Directly uses ATP
- Secondary Active Transport: Uses energy from one substance’s gradient to transport another
- Transport Diffusion:
- Cotransport: Substances move in the same direction
- Counter transport: Substances move in opposite directions
Clinical Manifestations of Meningitis
- Rapid and severe onset of symptoms
- Severe headache
- Photophobia (light sensitivity)
- Nuchal rigidity (hyperextended stiff neck)
- Increased ICP from brain edema and hypoxia leads to:
- Decreased alertness
- Loss of consciousness
- Changes in mental status
- Vomiting
- Seizures
Differentiate Decorticate vs Decerebrate
- Excitation injury may result from inability to meet metabolic demands of cells
Decorticate
- Abnormal flexion; due to increased flexor muscle excitability
Decerebrate
- Abnormal extension; due to increased extensor muscle excitability
Pathophysiology of Multiple Sclerosis
- Axon injury and formation of demyelinated plaques
Pathophysiology of Cerebral Palsy
- Altered central control of movement by the brain
Motor Dysfunction Classification
Spastic
- Inability of muscle to relax
- Hemiplegia: one arm and leg on the same side
- Diplegia: both legs
- Quadriplegia: all four extremities, trunk, and neck muscles
Athetoid or Dyskinetic
- Inability to control muscle movement
Ataxic
- Inability to control balance and coordination
Causes of Stroke
- Results from pathological events (shock, cerebral hemorrhage, ischemia, infarction)
- Leads to cerebral circulation impairment
- Risk factors: hypertension, smoking, diabetes
Differentiate Hemorrhagic vs Thrombolytic Stroke
Hemorrhagic Stroke
- Cerebral bleeding caused by trauma or defects in cerebral vessels
- Persistent hypertension and neoplasia can lead to vessel weakness and rupture
- Bleeding vessel compresses adjacent brain tissue and ventricles
Thrombolytic Stroke
- Caused by occlusions of cerebral artery
- Atherosclerosis forms most common site in the common carotid artery
Pathophysiology of Alzheimer’s Disease
- Accumulation of two abnormal proteins: amyloid beta and neurofibrillary tangles
- Neurofibrillary tangles: tau binds to microtubules for stability but becomes sticky and forms tangles
- Amyloid beta: fragment of amyloid precursor protein, forms plaques starting in small clusters then chains, finally organized as beta sheets
- Senile plaques: dense deposits of amyloid beta found outside neurons
Types of Seizures
Complex Seizures
- Involves both hemispheres; results in loss of consciousness; lack of memory during and after seizure
Simple Seizures
- Limited to originating hemisphere; can involve motor or sensory
Generalized Seizures
- Caused by generalized electrical transmission
- Absence seizures: brief change in LOC, eye/mouth movement; can occur up to 100x a day
- Myoclonic: involuntary movements, no LOC
- Tonic-clonic: convulsive; associated with tonic (continuous contraction) and clonic (rapid contraction-relaxation) motions
Signs of Meningitis and Precaution
- Symptoms include:
- Severe headache
- Photophobia
- Nuchal rigidity
- Increased ICP symptoms (decreased alertness, loss of consciousness, changes in mental status, vomiting, seizures)
Differentiate Para/Hemi/Quadriplegia
- Hemiplegia: involves one arm and one leg on the same side
- Diplegia: both legs
- Quadriplegia: all extremities, trunk, neck muscles
Clinical Manifestations of Migraines
- Pain: Unilateral, pulsing and throbbing
- Aura: Visual disturbances preceding headache
- Prodromal Symptoms: Mood changes, food cravings, constipation
Pathophysiology and Clinical Manifestations of Parkinson’s Disease
Pathophysiology
- Chronic, progressive neurologic condition
- Degeneration of pigmented dopaminergic neurons of the basal ganglia
- Impaired transport of dopamine
- Presence of Lewy bodies (proteins)
- Neuronal injury from oxidative damage suspected
Clinical Manifestations
- Tremor
- Involuntary quivering primarily in hands, arms, legs, face at rest
- Progressive onset
- Rigidity
- Jerky movements due to resistance from flexors and extensors
- Bradykinesia
- Associated with initiation of movement; may progress to akinesia (inability to move)
- Sudden halting of movement is a cardinal sign
- Postural instability
- Stiffness, decreased coordination, impaired balance
Early Signs of Increased ICP
- Change in mental status
- Headache
- Nausea/vomiting
- Visual disturbances
- Weakness
Generalized vs Tonic Clonic Seizure
Generalized Seizures
- Caused by generalized electrical transmission
- Absence seizures can occur up to 100x a day
Tonic-Clonic Seizures
- Convulsive; associated with tonic and clonic motions
Clinical Manifestations of Multiple Sclerosis
- Related to slowed nerve conduction
- Clinical Course Variations:
- Relapsing-remitting: periods of acute neurological symptoms with relief
- Primary progressive: chronic deterioration without exacerbations
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