pathology exam 2 based on study guide

What do nerve fibers do?

carry impulse from affected sites to the brain

What do A-delta fibers look like?

large/thick, middle of the three

What are A-delta fibers responsible for?

localized pain; ex: stubbing your toe

What does the activation of A-delta fibers cause?

Reflexive withdrawal; ex: touching something hot

How does pain travel on A-delta fibers?

they carry pain

What do C fibers look like?

thin, small, unmyelinated

What type of pain are C fibers responsible for?

dull, burning, tingling pain

What is an example of pain from C fibers?

chronic pain like back pain or burnt skin like chemical burns

How does pain travel on C fibers?

they carry pain

Are C fibers fast or slow?

slow

are delta fibers fast or slow?

fast

What do A-beta fibers look like?

big, large, thick; biggest of the three

What does activation of the A-beta fibers lead to?

closing the gate

What are A-beta fibers responsible for?

gate control theory; inhibit/decrease pain

How can A-beta fibers inhibit pain?

by overriding A-delta and C fibers through rubbing your finger/toe, etc

What is an example of A-beta fibers?

rubbing your knee, finger, etc after hitting it to stop pain

What are the 4 steps of nociception?

transduction, transmission, perception, modulation

What is transduction?

activation of pain receptors/excitatory neurotransmitters

What is substance P responsible for?

logging pain

What does transduction lead to?

initiation of action potential

What nerve fibers are responsible for the action potential?

A-delta and C fibers

When can modulation occur?

anywhere in the pain pathway depending on intervention

What is transmission?

traveling of pain signal from spinal cord to the thalamus to cortex perception

What is perception?

awareness of pain

What are the 3 systems involved with perception?

sensory, affective-motivational, and cognitive-evaluation

What is the sensory system responsible for (perception)?

intensity

What is the affective-motivational system responsible for (perception)?

emotional responses

What is the cognitive-evaluation system responsible for (perception)?

learning from experience

What is modulation of pain?

modification/alteration of the perception of pain

What could cause modulation of pain?

gate control theory, inhibitory/excitatory neurotransmitters, and opioid receptors/endogenous opioids

What is the pain pathway?

starts with a trauma which activates pain receptors (transduction), then the pain signal travels up to the spinal cord, thalamus, then the cortex (transmission), and finally there becomes awareness of the pain (perception); modulation can occur any time

When should you implement mediators of pain tolerance?

during perception/awareness

What are excitatory neurotransmitters?

glutamate, substance P, serotonin, histamine, bradykinin, and prostaglandins

What mediators can increase pain tolerance?

alcohol consumption, pain meds, hypnosis, warmth, distraction, and spirituality

What mediators can decrease pain tolerance?

prolonged pain, fatigue, anger, boredom, apprehension, and sleep deprivation

What is the gate control theory of pain?

pain can be inhibited through closing the gate by activating A-beta fibers

Can genetic diseases affect perception of pain?

yes

What is acute pain?

Short-term, self-limiting, stops after after injury heals

What are the types of acute pain?

somatic, visceral, referred

What is acute somatic pain?

arises from connective tissue, muscle, bone, and skin (surface)

What is acute visceral pain?

pain in the internal organs and abdomen (deeper)

What is referred pain?

pain felt in a part of the body other than its actual source

What are the clinical manifestations of acute pain?

anxiety, tachycardia, hypertension, increased BG, decreased GI acid secretion/motility, decreased blood flow to the skin and visceral organs, diaphoresis, dilated pupils, moaning/grimacing

What is chronic pain?

Persistent or recurring, lasts 6+ months, often difficult to treat

Is neuropathic pain acute or chronic?

chronic

What are some examples of chronic pain?

rheumatoid arthritis, osteoarthritis, and diabetic neuropathy

What are the effects associated with chronic pain?

mood and sleep

What are some examples of neuropathic pain?

diabetic neuropathy in feet, phantom limb syndrome, migraines, low back pain

What is a description of neuropathic pain?

burning, tingling (paresthesia), shooting, shock-like, stabbing, electricity

What does polygenic/multifactorial inheritance mean?

influence of multiple genes plus environmental factor

What are some examples of polygenic/multifactorial inheritance?

diabetes (DM), hypertension (HTN), schizophrenia, cancer, asthma

What does monogenic inheritance mean?

explained by single gene

What are the types of monogenic inheritance?

autosomal dominant, autosomal recessive, and x-linked

What does autosomal dominant mean?

both homozygous and heterozygous are affected --> every generation

What is an example of autosomal dominant?

Huntington's disease

What does autosomal recessive inheritance mean?

only homozygous are affected

What is an example of autosomal recessive?

sickle cell anemia

What does X-linked inheritance mean?

disease is carried on the X chromosome

What is an example of X-linked inheritance?

hemophilia

Are males or females more at-risk for X-linked disorders?

males

What is the pathophysiology of type 1 diabetes?

autoimmune injury, no insulin, total destruction of beta cells, and under 35 for diagnosis, weight loss

What are the genetics of type 1 and type 2 diabetes?

polygenic/multifactorial

What lab results would you see for fasting type 1 and type 2 diabetes?

over 126 mg/dL

What lab results would you see casually/anytime for type 1 and type 2 diabetes?

over 200 mg/dL and symptoms

What HgA1C would you see in type 1 and type 2 diabetes?

over 6.5% HgA1C

What are the signs/symptoms of type 1 diabetes?

polyuria, polydipsia, polyphagia

What are the signs/symptoms of type 2 diabetes?

r/t lifestyle and nonspecific; diet with increased carbs and sugar and obesity

What are the risk factors for diabetic ketoacidosis (DKA)?

type 1 diabetes and stress

Why is stress a risk factor for type 1 diabetes?

cortisol is a glucucorticoid so increased cortisol means you'll have more blood glucose absorption

What is the pathophysiology of DKA?

Ketones develop from breakdown of fat, lots of hydrogen leads to metabolic acidosis, and hyperglycemia causes increased urination and therefore dehydration

What are the signs/symptoms of DKA?

potassium alterations (increase r/t acidosis and decrease r/t osmotic diuresis), hypotension and tachycardia, Kussmaul breathing, and acetone breath

What are the complications of DKA?

hypovolemic shock

What are the risk factors for HHNKS?

uncontrolled type 2 diabetes

What is the pathophysiology of HHNKS?

hyperglycemia leads to osmotic diuresis (increased urination) and dehydration

What are the signs/symptoms of HHNKS?

polydipsia, polyuria, increased BG, hypokalemia, and confusion due to low perfusion to the brain

What are the complications of HHNKS?

hypovolemic shock

What is DKA?

diabetic ketoacidosis

What is HHNKS?

hyperglycemic hyperosmolar nonketotic syndrome

What are the main differences between DKA and HHNKS?

DKA has Kussmaul's, hyperkalemia, and ketones/acidosis

What are the signs and symptoms of hypoglycemia?

HANGRY and SNS activation

What are the HANGRY signs/symptoms of hypoglycemia?

irritability, headache, dizziness, fatigue, weakness

What are the SNS activation signs/symptoms of hypoglycemia?

shaky, tachycardia, sweaty, anxious

When is the polyol pathway used?

when some tissues do not require insulin for glucose transport

How does the polyol pathway work?

when there is increased BG using the polyol pathway it can get overwhelmed and its byproducts accumulate leading to increased osmotic pressure, edema, and cell damage

What byproducts are made from BG in the polyol pathway?

fructose and sorbitol

What are the outcomes of overusing the polyol pathway?

increased osmotic pressure, edema, and cell damage; can lead to blood vessels bursting in eyes (retinophathy)

Does the polyol pathway occur naturally?

yes

What could cause primary hyperthyroidism?

thyroid tumor or autoimmune = Graves' Disease

What labs would you see with primary hyperthyroidism?

high TH and low TSH

What could cause secondary hyperthyroidism?

AP tumor

What labs would you see with secondary hyperthyroidism?

high TSH, high TH

What are the signs/symptoms of hyperthyroidism?

CNS: insomnia, restless, distractible
Metabolism: weight loss, hungry, heat intolerance
CV: increased HR and CO, sweating

What could cause primary hypothyroidism?

thyroid damage, autoimmune = hashimoto disease

What labs would you see with primary hypothyroidism?

low TH, high TSH

What could cause secondary hypothyroidism?

AP tumor

What labs would you see with secondary hypothyroidism?

low TSH, low TH

What are the signs/symptoms fo hypothyroidism?

CNS: lethargic, fatigue
Metabolism: weight gain, cold intolerance
CV: bradycardia, low BP, constipation, hair loss

What is thyroid storm?

rare but if a person has undiagnosed hyperthyroidism and is under stress, it could lead to super severe hyperthyroidism

What could cause primary hyperparathyroidism?

tumor in the parathyroid

What labs would you expect to see with primary hyperparathyroidism?

high PTH, high calcium