Week 3 Endocrine Flashcards
T/F: Gout is more common in men than women?
True
Prevalence increases with age, >65
Gout considered a musculoskeletal disorder or metabolic disorder?
Both
Metabolic disorder b/c of purine metabolism
Musculoskeletal disorder b/c monosodium urate crystal deposition in and around joints.
What are some risk factors of Gout?
- Positive Family History
- Older Age
- Male
- Overweight
- Other chronic conditions (CKD, Hypothyroidism, Infections)
- Post-surgery
- Some Medications (E.g. Diuretics, low dose ASA)
- Alcohol
Etiology of Gout: Primary vs Secondary
Primary - High levels of uric acid result from either increased production or decreased excretion rates of uric acid
Secondary - Hyperuricemia results from primary disease processes such as HTN, HF, kidney disorders.
What medications can induce hyperuricaemia or gout?
Diurectics, ASA, ETOH, nicotinic acid, ethambul (anti-TB), pyrazinamide (anti-TB).
Drugs raise serum uric acid level by increasing uric acid reabsorption and/or decreasing uric acid secretion in gout.
Adequate hydration and routine uric acid level monitoring should be encouraged for drugs known to induce hyperuricaemia.
Drugs are FACT
- Furosemide
- Aspirin, alcohol
- Cyclosporin
- Diurectics (loop diuretics, thiazide diuretics and thiazide-like diuretics)
Pathophysiology of Gout
Uric acid can be obtained from the diet or made endogenously by xanthine oxidase, which converts xanthine to uric acid
An excess of uric acid results in hyperuricemia
Uric acid can deposit in the skin/subcutaneous tissues (tophi), synovium (microtophi), and kidney, where they can crystalize to form monosodium urate crystals that lead to gout
Uric acid crystals trigger an inflammatory response
Stages of Gout - initial phase:
Acute gouty arthritis
-sudden onset; maximal severity of the flare reached within 12-24 hours
-attack will subside spontaneously within 5-10 d; may recur
-red, hot, painful to touch, swollen
Stages of Gout - in between phase:
Intercritical gout (period without flares)
*pain free
Stages of Gout - chronic phase:
Chronic/tophaceous gout
*progression of gout has been inadequately treated resulting in urate crystal deposits (tophi) in the joints that can cause deformity and disability of the joint
Onset of gout flares at night or during the daytime?
night time
What joint is normally affected?
Base of great toe metatarsophalangeal joint or knee
*initial normally affects single joint (80%)
*polyarticular flares (20%) of initial flares with increased reoccurrence with untreated gout
What is the difference btwn gout flare and cellulitis?
limited mobility with gout
mobility is preserved with cellulitis unless infection over a joint
What connective tissues can urate crystals (tophi) be deposited?
cartilage, tendons, bursae, soft tissues, and synovial membranes
What are the common sites of urate deposits?
first MTP, ear helix, olecranon bursae, tendon insertions (common in Achilles tendon)
What are some medical complications that can arise from or be worsened by obesity?
DMT2, gallbladder disease, NAFLD, gout
Excess and ectopic body fat are important sources of adipocytokines and inflammatory mediators that can alter glucose and fat metabolism, leading to increased cardiometabolic and cancer risks, and thereby reducing disease-free duration and life expectancy by ____to _____ years.
6 to 14 years.
It is estimated that 20% of all cancers can be attributed to obesity, independent of diet.
Obesity increases the risk of the following cancers:
Colon (both sexes)
Kidney (both sexes)
Esophagus (both sexes)
Endometrium (women)
Postmenopausal breast (women)
People living with obesity experience something that contributes to increased morbidity and mortality, and it is independent of weight or BMI. What is it?
Pervasive weight bias and stigma.
What are the 5 A’s for obesity management in adults?
Ask - would it be alright if we discussed your weight?
Assess - Value-based goal that matters to the patient, obesity classification, adiposity-related complications, disease severity
Advise - discuss obesity risks, health benefits of obesity management
Agree - on realistic expectations, sustainable behavioural goals and health outcomes. Agree on a personalized action plan.
Assist - identify drivers and barriers, provide education and resources.
There are 4 medications approved for use in obesity management in Canada (as per Cdn guideline). What are they?
There are four medications indicated for long-term obesity management in Canada as adjuncts to health-behaviour changes:
liraglutide (Saxenda®),
naltrexone/bupropion (Contrave®) in a combination tablet,
orlistat (Xenical®) and
semaglutide (Wegovy®).
All four medications are effective in producing clinically significant weight loss and health benefits greater than placebo over a duration of at least one year.
Obesity medications are intended as part of a long-term treatment strategy. Clinical trials of pharmacotherapy for obesity management consistently demonstrate regain of weight when treatment is stopped.
True or false?
True!
According to the Cdn guideline, when should you consider treating obesity with pharm?
Pharmacotherapy for obesity management can be used for individuals with BMI ≥ 30 kg/m2 or BMI ≥ 27 kg/m2 with adiposity-related complications, in conjunction with medical nutrition therapy, physical activity and/or psychological interventions.
What is the recommended management approach if your patient has severe mental illness and is gaining significant weight assoc. with their anti-psychotic medications?
Metformin + psychological tx such as CBT
T/F: Vitamin C is recommended for prevention of acute gout attacks?
False. Not effective in lowering serum uric acid levels.
Is a low calorie diet just as acceptable and beneficial if not more than a low purine diet to reduce the risk or frequency of gout flares?
Yes. Recommend one less portion of meat or seafood per day.
Encourage low-fat or non-fat dairy products & vegetables
it can be impossible for patients to limit their purine intake enough to significantly alter their risk of a gout flare, and dietary restrictions could result in other nutritional deficiencies.
An excess of uric acid is called hyperuricemia. How does uric acid even develop?
Uric acid can be obtained from the diet (break down purine) or made endogenously by xanthine oxidase, which converts xanthine to uric acid
Purine is naturally occurring in our body, but is also found in certain foods
- A purine-rich diet can ↑ serum uric acid by 1 to 2 mg/dL (~60 to 120umol/L)
What foods are high in Purine?
Food is SALT (S)
Seafood
(Avoid sardines, shellfish)
Alcohol
(Avoid alcohol overuse: >2 servings/day in males & > 1 serving/day in females; limit beer)
Liver and Kidney
(Avoid high-purine organ meats; limit beef, lamb, pork,)
Turkey
Syrups/sugars, sweetened sodas
(Avoid high fructose corn syrup sweetened sodas, beverages, or foods; Limit naturally sweet fruit juices, table sugar, sweetened beverages & desserts, table salt (including in sauces & gravies)
What are the differentials of Gout?
Infectious arthritis.
Hyperparathyroidism.
Pseudo gout (commonly occurs in the knee wrist or other joint, bursitis)
Cellulitis.
Bursitis
When is it appropriate to draw a serum urate blood test when assessing for gout?
Blood test: urate levels may or may not be elevated in a flare – most accurate time for assessment of serum urate is at least 2 weeks after a flare
What is the mechanism of an antihyperuricemic drug?
decrease uric acid production by inhibiting xanthine oxidase. Start low and titrate up.
Use when maintaining or preventing further flare ups.
When would you consider starting an antihyperuricemic drug?
*>2 attacks/year, bone erosions/arthritis
*chemotherapy
*sUA >800 umol/L
* advanced dx tophus/tophi or radiographic damage or urolithiasis;
*CKD >Stage 2
What is first line treatment when maintaining gout flares?
Allopurinol
What is treatment for acute gout flares?
Rapid treatment initiative - within 24hrs
Colchicine, NSAIDs, or corticosteroids all 1st-line & effective;
consider CI/DI/AE. Start at high dose, then taper.
From Gayle’s pres in 543:
An example for a patient with 4 gout attacks per year, decision made to start prophylaxis:
Colchicine 1.2 mg x 1 stat, then 0.6 mg x 1 hr on day #1
– Then Colchicine 0.6 mg daily for 3 months
– Start allopurinol 100mg daily 10 days after acute gout flare
– Titrate up by 100mg every 2 weeks, up to 300mg daily and R/A
– Allopurinol 300mg daily is a common dose
Or
Ibuprofen 600mg TID with Pantoprazole 40mg daily for 7 to 14 days
– Then Ibuprofen 400mg BID or TID for 3 months, preferably with PPI for GI protection.
– Start allopurinol 100mg daily 10 days after acute gout flare
– Titrate up by 100mg every 2 weeks, up to 300mg daily and R/A
– Allopurinol 300mg daily is a common dose
ASA and thiazide are risk factors? Do you still prescribe if someone is high risk CV disease?
Yes
Are glucocorticoids useful in treatment of gout?
Yes. Decreases pain and inflammatory response; effective for gout equal to NSAIDs. Useful if CI/AE to NSAIDs or colchicine e.g. renal, transplant, warfarin pts, etc.
May add acetaminophen for pain
When treating an older adult, what is the recommended starting dose as well as titration dose when prescribing allpurinol?
If CKD , hepatic impairment , or elderly,
initiate at 50mg po daily cc & increase by 50mg q2-4wks.
If an older adult is complaining of weakness and functional decline with history of gout, what investigations should be completed? (if they are on colchicine)
Colchicine – myopathy and peripheral neuropathy can be subtle in older adults, although brief courses (eg, less than a week) for gout flares should not be associated with these complications.
- In case of longer courses or frequent use, complaints of weakness and functional decline while taking colchicine should prompt a careful neurologic examination, laboratory evaluation including a serum creatine kinase, and empirical drug discontinuation
What are the contraindications of NSAIDS in older adults?
Heart failure, kidney dysfunction, or gastrointestinal disease.
In the absence of such contraindications, indomethacin in older adults because of the greater risk of adverse effects with this medication compared with other NSAIDs.
Can we prescribe glucocorticoids to older adults?
Brief courses of oral glucocorticoids are generally tolerated in patients in whom NSAIDs or colchicine may pose an increased risk.
What is another name for pseudogout?
calcium pyrophosphate dihydrate (CPPD) Disease
What is CPPD disease?
An acute inflammatory condition primarily affecting the larger joints in which crystal deposits occur in the connective tissues
What connective tissue CPPD primarily attack?
synovial membrane/joint
crystal formation in the cartilage that shed into joint
Is CPPD painful?
Not always - can clinically present like urate gout but pt can be asymptomatic to painful attacks. Majority of individuals are asymptomatic.
Acute attacks of CPPD can happen more often in women than men?
Men more often have acute attacks
Women with OA and CPPD may have a higher incidence of occurrence
“OA with CPPD is the most prevalent form of symptomatic CPPD disease. Approximately 50% of patients with symptomatic CPPD disease show progressive joint degeneration of multiple joints. This pattern of disease is referred to as “pseudo-OA” because of its resemblance to OA occurring in the absence of CPPD. Approximately 50% of such patients, episodes of acute inflammation typical of pseudogout punctuate the course, but for the rest joint degeneration proceeds by a process more typical of classical OA.”
Is gout associated with CPPD disease?
Can be…approximately 5% of patients have gout with CPPD disease.
What are the consequences of CPPD deposits?
*Acute inflammatory arthritis
*Inflammatory and degenerative chronic arthropathies
*Radiographic cartilage calcification and constitute the spectrum of CPPD disease (Rosenthal, 2018a).
Radiographic calcification is commonly seen in patients with CPPD, but is not specific, and therefore not pathognomonic.
Risk Factors of CPPD?
- Idiopathic
- Older age
- Joint trauma
- Hospitalization/illness
- Familial chondrocalcinosis
- Endocrine/metabolic disorders: gout (5%), hyperparathyroidism, hemochromatosis, hypophosphatasia, hypothyroidism, hypomagnesaemia, Gitleman’s syndrome, hemosiderosis
Age group who primarily is affected with CPPD?
50% of cases in those older than 84; 36% in ages 75-84; 15% in age 65-74
Which joint is primarily affected with CPPD?
Joints affected: knee approximately 50% of the time. Others: wrists, shoulders, ankles, feet and elbows.
Why is CPPD difficult to diagnose?
Can mimic other types of arthritis including gout, rheumatoid arthritis, osteoarthritis, and neuropathic joint disease.
What is asymptomatic CPPD disease?
Most joints in which CPP crystal deposition is apparent on x-ray are asymptomatic. This is true even among patients in whom acute or chronic clinical manifestations of CPPD disease in 1 or more other joints has occurred. However, with targeted questioning, these patients with apparent asymptomatic CPPD may be found to have manifestations of an arthritic disorder.
What are the precipitating events for acute CPPD disease?
- Trauma, surgery, or severe medical illness often provoke acute attacks.
- In particular, flares of acute CPP crystal arthritis after parathyroidectomy have been observed, perhaps due to associated precipitous changes in calcium and magnesium levels.
Three types of CPPD disease that Don wants us to understand.
Asymptomatic CPPD disease; Acute CPPD arthritis; Chronic CPP crystal arthritis
S&S of Acute CPPD arthritis?
Characterized by self-limited acute, or subacute, attacks of arthritis involving 1 or several extremity joints.
S&S of severe acute inflammation with intense pain, redness, warmth, swelling, and joint disability.
There can also be inflammation of several adjacent joints (cluster attacks) or petite attacks (minimally painful episodes of joint warmth and swelling) (Rosenthal et al., 2018b).
How to decipher btwn CPPD and urate gout?
In order to help differentiate CPPD from urate gout, think location and duration of symptoms.
LOCATION
- The knee is affected in >50% of all acute attacks of CPPD, while the 1st MTPJ is most frequently affected in urate gout.
- Other joints typically affected in acute CPP crystal arthritis include wrists, shoulders, ankles, feet, and elbows.
- An upper extremity site of inflammation (wrist, elbow, shoulder) for a first attack should raise suspicion for acute CPPD arthritis
DURATION
Initial episodes of acute CPPD may persist longer before remitting than do episodes of urate gout, which typically last 1-2 weeks.
CPPD rarely have visible masses of crystals in synovium and adjacent joint structures, resembling gouty tophi.
- These masses can cause local pain/compressive symptoms.
Associated symptoms r/t Acute CPPD arthritis?
- Low grade fevers and elevated ESR
What is chronic CPP crystal arthritis?
The term pseudo-rheumatoid arthritis has been used to describe a non-erosive, inflammatory arthritis in which CPP crystals are demonstrated in joint fluid.
Chronic CPP occurs in ≤5% of patients with symptomatic CPPD, and most of those are older adults
S&S of chronic CPP crystal arthritis?
*Resembles RA, with significant morning stiffness, fatigue, synovial thickening, localized edema, and restricted joint motion, due either to active inflammation or to flexion contractures.
*Systemic features of leukocytosis, fever, mental confusion, mimicking sepsis is also seen.
Primary locations of chronic CPP crystal arthritis?
*Multiple joints, frequently in peripheral joints of the upper and lower extremities, (wrists and MCPJs), as well as the knees and elbows.
*Usually symmetric.
Duration of chronic CPP crystal arthritis?
*Articular inflammation may last several months.
*Inflammation of the various joints involved tends to wax and wane independently of one another.
**This is in contrast to RA, where synchronous flare and remission are typical.
*Episodes are self-limited, lasting days to weeks.
What is the most prevalent form of CPPD Disease?
OA with CPPD
Progressive joint degeneration of multiple joints - ‘pseudo-OA’
Location of OA with CPPD?
*Knees are most often affected, followed by the wrists, MCPJs, hips, shoulders, elbows, and spine.
*Pattern is frequently symmetric, but unilateral or more severe degenerative change unilaterally, is also found.
*Typically involves same joints as in OA (interphalangeal joints of the hands, the 1st CMCJ, the knees, or the 1st MTPJ.)
**The first carpometacarpal joint (CMCJ) is located at the base of the thumb, where the metacarpal bone of the thumb articulates with the trapezium bone of the wrist.
*An etiologic or accelerating role for CPP crystal deposition in joint degeneration seems likely when radiographic calcification is present early in the course of degeneration, particularly if the degenerative changes also involve joints atypical for OA (wrists, MCP joints, elbows, and shoulders) in the absence of a preceding history of joint trauma or stress.
S&S of OA with CPPD?
- Clinical examination of individual joints does not typically differ from those observed in OA:
- asymmetric bony enlargement
- tenderness
- effusions
- crepitus
- restricted joint motion.
- Patients also develop contractures of involved joints and valgus deformities of the knees.
Diagnosis criteria of CPPD?
Suspected in the patient:
- most often > 65
- with acute or subacute attacks of arthritis (particularly of the knee),
- arthritis similar in character to RA or OA,
- apparent CPPD crystal deposition on radiographs
- in patients with other selected but less common presentations (Rosenthal et al., 2018b).
Diagnosis is largely based upon the demonstration of CPP crystals in tissue or synovial fluid and/or upon radiographic evidence of the disease.
Generally, differences between the patterns of joint involvement in urate gout and acute CPP crystal arthritis are insufficient to permit definite diagnosis without demonstration of the specific crystal in the inflammatory joint effusion.
Differentials of CPPD?
Gout
Septic arthritis
OA
RA
What imaging is recommended to help diagnose CPPD?
Radiography, US, or CT - MRI not sensitive enough
Imaging reveals:
*evidence of cartilage calcification (chondrocalcinosis)
*degenerative changes in the joint
After determining the type of crystal in tissue fluid and /or radiographic evidence, and there is a positive diagnosis of calcium CPPD disease, what other conditions should you investigate then?
- hemochromatosis
- hyperparathyroidism,
- hypomagnesemia,
- hypophosphatasia,
- familial hypocalciuric hypercalcemia (FHH)
When investigating associated conditions what BW should you order?
- Calcium,
- Phosphorous
- Mg
- parathyroid hormone (PTH)
- ALk. Phos.
- Ferritin
- iron and transferrin.
Does a patient require treatment if asymptomatic and cartilage calcification was noted on xray?
no
Management for acute CPPD arthritis?
- Supportive measures for symptom relief – ice, rest, analgesic medications
- Usually anti-inflammatory therapy
- intraarticular glucocorticoid injections preferred if small number of joints
- Systemic NSAIDS or oral glucocorticoids or colchicine if multiple joints or joints that cannot be injected
- Prophylaxis with colchicine or NSAIDs if more than three acute events annually
Management for chronic CPPD?
Primarily NSAIDs, other considerations are colchicine, low-dose oral steroids, hydroxychloroquine
True or false: insulin secretion acts on a positive feedback loop.
False.
What are the risk factors for developing T2DM?
Family history of T2DM
CVD risk factors (High BP, High cholesterol, High BMI or overweight)
Prediabetes (impaired glucose tolerance or impaired fasting glucose)
Presence of EOD associated with DM
Conditions or meds associated with DM (PCOS, Psychiatric disorder (schizophrenia, depression, bipolar- meds assoc with DM), OSA, Glucocorticoid use
What is the diagnostic criteria for T2DM? (Include A1C and FBG cut off)
A1C 6.5 or greater
FPG 7 or greater
If asymptomatic and A1C or FPG in diabetes range, repeat the same test as confirmatory test.
If both FPG and A1C are available and only one is in the diabetes range, repeat the test in the diabetes range as the confirmatory test.
If both FPG and A1C are available and both are in the DM range, DM is confirmed.
If symptomatic, dx can be determined with one test.
If a patient is asymptomatic and their A1C is 6.6 , can you diagnose them with DM?
Nope. Not unless they also have a FPG in the DM range.
Repeat A1C as confirmatory test.
See QRG p1
At what age do we start screening for DM?
Age 40+ (or earlier if presence of risk factors)
If a patient has no risk factors for DM, how often do you screen them?
q3 years
If a patient has presence of risk factors for DM (or very high risk), how often do you screen them?
q6-12 mo
What is impaired fasting glucose
FPG 6.1- 6.9 (no caloric intake for 8h0
What level of FPG is diagnostic for DM?
FPG 7+
What is prediabetes
A1C 6-6.4
What level of A1C is diagnostic of DM?
A1C 6.5+
What is the target for glycemic control for functionally dependent older adults?
A1C 7.1- 8.0
What is the target for glycemic control for recurrent severe hypoglycemia or hypoglycemia unawareness?
A1C 7.1- 8.5
What is the target A1C for frail elderly/ those with dementia?
A1C 7.1- 8.5
For repetition sake, outline the A1C targets for older adults who are:
-functionally dependent
-experience recurrent severe hypoglycemia or hypoglycemia unawareness
-are frail or have dementia
-functionally dependent 7.1-8.0
-experience recurrent severe hypoglycemia or hypoglycemia unawareness 7.1-8.5
-are frail or have dementia 7.-8.5
What is the focus in DM management when treating an older adult with multiple comorbidities or hypoglycemia?
PREVENT HYPOGLYCEMIA
What DM drugs are most strongly associated with hypoglycemia
Sulfonylureas (gliclazide, glimepiride, glyburide)
Insulin
True or false- if you must use a SU, intial doses in the older person should be half of those used in younger person, and doses increased more slowly
True
George must be treated with a sulfonylurea for his T2DM. Which SU is the most strongly associated with hypoglycemia
Glyburide
Gliclazide and gliclazide MR [Grade B, Level 2] and glimepiride [Grade C, Level 3] should be used instead of glyburide, as they are associated with a reduced frequency of hypoglycemic events
Sherry requires insulin for her DM. What is the best kind to start with?
Long acting! (Detemir, glargline)
Try to avoid NPH, 30/70 to lower frequency of hypoglycemic events.
How can you prevent insulin dosing errors in the older adult?
In older people, premixed insulins and prefilled insulin pens should be used to reduce dosing errors and to potentially improve glycemic control [Grade B, Level 2].
True/ false: Sliding scale insulin should be used in LTC, as it provides more accurate control of glucose to keep patient A1C within the 7.1-8.5 range.
FALSE
Sliding scale (reactive) and correction (supplemental) insulin protocols should be avoided in elderly LTC residents with diabetes to prevent worsening glycemic control [Grade C, Level 3].
Randy is a 70 year old man newly diagnosed with diabetes. He has no medical comorbidities and lives independently at home with his partner. He is functionally independent. What should his target A1C be?
7 or less
Older adults who are otherwise well, independent and have at least a decade of healty life expectancy should be managed as general adults.
True or false- A1C naturally increases with age.
True!
We are encouraged to use FPG and A1C in screening.
True or false- screening for DM is appropriate for an 83 year old.
Consider life expectancy.
Diabetes Canada guidelines: Make the decision for the appropriateness of screening based on the individual – unlikely to be beneficial for age > 80
Gemma is a 75 year old living in the suite of her daughters house. Her daughter cooks all her meals for her, does all her finances and shipping, and occasionally helps Gemma get dressed or bathe if she is having a hard time due to OA pain. Gemma also has T2DM. What is an appropriate A1C target for her?
Functionally dependent
7.1-8
Carlo is a frail 72 year old individual. What is his A1C target?
7.1- 8.5
What test can be used to predict with older adults will have difficulty learning to inject insulin?
The clock drawing test may be used to predict which older individuals will have difficulty learning to inject insulin [Grade C, Level 3].
True or false- a DPP$ inhibitor should be used over sulfonylureas as second line therapy to metformin.
True
a. DPP-4 inhibitors should be used over sulfonylureas as second-line therapy to metformin because of a lower risk of hypoglycemia [Grade B, Level 2]
True or false- diabetic diets are an important way to manage T2DM patients in LTC
False
12. In older LTC residents, regular diets may be used instead of “diabetic diets” or nutritional formulas [Grade D, Level 4].
Describe some ways that T2DM presents in old age compared to the “classic” presentation in middle age adults.
-Old adults tend to be thin or have mild visceral obesity (middle aged tend to be obese)
-Glucose induced insulin release is low (middle age- increased, but insufficient to overcome insulin resistance)
-Older adults often have dehydration instead of polydipsia
-Polyuria may present as incontinence
-Other presenting symptoms may include dry eyes, dry mouth, confusion, incontinence, or diabetic complications
-Older adults may occasionally present with hyperosmolar non ketotic coma
What does de-prescribing involve?
o Stopping medications
o Switching to safer medications
o Lowering doses
What are some factors to consider when de- prescribing for T2DM?
glycemic targets, goals of care, and time to benefit.
Name some populations we de-prescribe for in T2DM
- De- prescribe (no benefits for tight glycemic control) in older adults who are frail, have cognitive impairment or dementia, or limited life expectancy (<5 years).
- De-prescribe antihyperglycemics in those at risk of hypoglycemia (see above bullet, plus those with overly intense glycemic control, multiple comorbidities, drug interactions, hypoglycemia history, hypoglycemia awareness, impaired renal function)
Describe some common de-prescribing strategies for T2DM meds
- De- prescribe agents known to contribute to hypoglycemia (esp. sulfonylureas, insulin)
o Of the sulfonylureas, glyburide is the worst (switch to gliclazide or non- SU)
o Switch NPH or mixed insulin to detemir or glargine.
What are the consequences of hypoglycemia?
Consequences of hypoglycemia include impaired cognitive and physical function, falls, fractures, MVAs, seizures, ED visits, hospitalization, and death
What are common symptoms of hypoglycemia in older adults?
dizziness, weakness, delirium, confusion
What are diabetic autonomic neuropathies?
affect the autonomic neurons and may target the innervation of the heart (cardiac autonomic neuropathy, gastrointestinal tract, genitourinary system, sexual function, pupillary responses and sweating.
Occurs in at least 30% of T1DM after 20 years and may be present in up to 60% of people with type 2 diabetes after 15 years
What kind of sensations are normally felt first with diabetic peripheral neuropathy? What fibres does this involve?
What is the classic distribution of symptoms?
most common early symptoms are from small fibre involvement and include pain (e.g. sharp, shooting) and dysesthesias (e.g. burning)
Symmetric stocking & glove distribution is typical
Usually affects feet before hands
involvement of large fibres may cause numbness, tingling and loss of protective sensation
T/F only sensory neurons are affected by diabetic peripheral neuropathy
F - Can affect motor, sensory, and autonomic nerve fibres
Motor neuropathies less common than sensory but can affect muscle groups, particularly of the feet, contributing to deformity and unstable balance
may see loss of motor nerve function with clawed toes and small muscle wasting in hands and flexor muscles
Patients with DM should be screened yearly for neuropathies, even if they are asymptomatic.
What screening tests should you do for someone who is asymptomatic?
Asymptomatic screening for neuropathy can be performed rapidly and reliably using the 10 g monofilament or the 128 Hz tuning fork over the dorsal aspect of the great toe bilaterally
Other screening tests can include pinprick or temperature (starting distally bilaterally and moving proximally until a sensory threshold is identified) and ankle reflexes.
Evaluation for neuropathy in the lower limbs should also accompany the evaluation of vascular supply and skin integrity
What is the most common symptom of diabetic autonomic neuropathy?
Erectile dysfunction is the most common symptom of DAN (up to 40%)
Outline the procedure for rapid screening for neuropathy suing the 128Hz vibration tuning fork
- Strike the tuning fork on the palm of your hand (hard enough that it will last about 40 sec)
- Apply the base of the tuning fork to the patient’s forehead of sternum and ensure the vibration sensation (not just touch) is understood
- With the patient’s eyes closed, apply the tuning fork to the bony prominence at the dorsum of the first toe just proximal to the nail bed. Ask if the vibration sensation is perceived.
- Asked the patient to tell you when the vibration stops, then dampen the tuning fork with your other hand
- One point is assigned for each vibration sensation perceived (vibration “on”) . Another point is assigned if the correct timing of dampening of the vibration is perceived (vibration “off”)
- Repeat this procedure again on the same foot, then twice on the other food in an arrhythmic manner so the patient doesn’t anticipate the stimulus being applied
Outline the procedure for rapid screening of diabetic neuropathy using monofilament testing
- Show the monofilament to the patient. Touch it to the patient’s forehead of sternum so the sensation is understood
- Instruct the patient to say “yes” every time the monofilament stimulus is perceived
- Get patient to close eyes. Apply to dorsum of of great toe proximal to nail bed (like the tuning fork). Use smooth motion to touch the skin, bend the filament for a full second, then lift from the skin.
- Perform this 4 times per foot in arrhythmic manner
For each of the 8 stimuli, apply score of 0 if not percieved, 0.5 if percieved but much less than on sternum/forehead, and 1 if felt normally.
- Score of 3/8 means the presence of neuropathy is likely
- Score 3.5-5/8 means risk of onset of neuropathy in lext 4 years is high
- score of 5.5 of greater means low risk of neuropathy in next 4 years
Outline the PROCEDURE FOR MONOFILAMENT TESTING IN THE DIABETIC FOOT (this is for someone who is having symptoms of neuropathy and you’re wanting to see if their protective sensation is intact)
Sensory examination should be carried out in a quiet and relaxed setting
First apply the monofilament on the patient’s hands (or elbow or forehead) so that he or she knows what to expect.
The patient must not be able to see whether or where the examiner applies the filament
The three sites to be tested on both feet are indicated below (Figure 1)
Apply the monofilament perpendicular to the skin surface (Figure 2a).
Apply sufficient force to cause the filament to bend or buckle (Figure 2b).
The total duration of the approach – skin contact and removal of the filament – should be approximately 2 seconds.
Apply the filament along the perimeter of, not on, an ulcer site, callus, scar or necrotic tissue.
Do not allow the filament to slide across the skin or make a repetitive contact at the test site.
Press the filament to the skin and ask the patient whether they feel the pressure applied (‘yes’/’no’) and next whether they feel the pressure (‘left foot/’right foot’).
Repeat this application twice at the same site, but alternate this with at least one ‘mock’ application in which no filament is applied (total three questions per site).
Protective sensation is present at eac site if the patient correctly answers two out of three applications. Protective sensation is absent with two out of three incorrect answers – the patient is then considered to be at risk of ulceration.
Encourage patients during testing by giving positive feedback.
What are the pillars of management of diabetic neuropathy?
NO CURE
Proper foot care, including daily foot inspection
Effective blood glucose control
Medications that may help with nerve pain
What is hyperparathyroidism? What electrolyte is imbalanced here?
Primary hyperparathyroidism (PHPT) is characterized by hyperactivity of one or more parathyroid glands, disordered calcium homeostasis, and an increase in serum calcium with elevated, or inappropriately present, circulating levels of parathyroid hormone (PTH)
The acronym RHINOS is helpful in guiding your diagnostic reasoning about possible etiology for hypercalcemia. What does this stand for?
R: renal insufficiency
H: hyperparathyroidism
I: immobilization and iatrogenic
N: neoplasms
O: other endocrinopathies (MEN 1 and 2)
S: sarcoidosis
It is still common to hear clinicians in practice talk about hyperparathyroidism as a condition of: bones, stones, thrones, moans & groans, and psychiatric overtones.
What the heck does this mean?
Refers to the signs and symptoms of hypercalcemia
“Groans” - constipation and muscle weakness from decreased contractility
“Stones” - calcium based kidney/gallbladder stones
“Thrones” - (refers to a toilet) polyuria due to impaired sodium, water absorption
“Bones” - pain from chronic demineralization
“Psychiatric Overtones” - depressed mood, confusion
Which pneumonia vaccines are recommended for older adults? In what order should they ideally be administered?
Pneumococcal conjugate (PCV13; Prevnar) and pneumococcal polysaccharide (PPSV23) are also indicated for all persons age 65 or older
Ideally, PCV13 should be administered first, with PPSV23 administered 1 year later for immunocompetent patients and 8 weeks later for immunocompromised patients.
If a patient has already received the PPSV23, PSV13 should be administered 1 year later.
A second immunization of PPSV23 can be administered for patients age $ 65 years at 5 years from the first vaccination, with at least 1 year from the PCV13 vaccination
What is really important to consider as a cause of dizziness in older adults?
cardiac causes
In a study of those 65-95 years old, 69% of those with dizziness had presyncope-type dizziness and underlying cardiovascular disorder was the contributing factor in 57%, followed by peripheral vestibulopathy (14%) and psychiatric conditions (10%)
Where does central vertigo originate? Common causes?
Brainstem/cerebellum
Etiology: tumor, stroke, drugs, MS
Where does peripheral vertigo originate? Common causes?
Inner ear or vestibular nerve
Idiopathic
Meniere’s
Benign paroxysmal positional vertigo
Acoustic neuroma
Trauma
Drugs – aminoglycoside toxicity
Labyrinthitis
Herpes zoster oticus (Ramsay Hunt syndrome)
Otitis media
Meniere’s
How long do episodes of dizziness last?
Key accompanying symptoms?
Recurrent episodes, lasting several minutes to hours
Spontaneous onset
Episodes may be preceded by ear fullness/pain, accompanied by vertigo, unilateral hearing loss and tinnitus
Audiometry shows unilateral low-frequency hearing loss
BPPV
length of episodes
What precipitates an episode typically?
Recurrent episodes, brief (SECONDS)
Predictable head movements or positions precipitate symptoms
How do we diagnose and treat BPPV?
Dix-Hallpike maneuver diagnostic
Treated with Epley maneuver
Define vertigo
illusion of rotational, linear, or tilting movement of self or environment
Differentiate central vs peripheral vertigo with regard to auditory symptoms. Common in one or both or neither?
Common in peripheral
Rare in central
Differentiate central vs peripheral vertigo with regard to neurological symptoms. Common in one or both or neither?
Common in central
Rare in peripheral
How does nystagmus present differently in peripheral vs central causes of vertigo?
Peripheral: Unidirectional
Horizontal or rotatory
Central: Bidirectional
Horizontal or vertical
How long do episodes of vertigo last in labrynthitis/vestibular neuritis?
And while you’re at it, remind me of how long episodes last in BPPV & menieres?
Labyrinthitis/
Vestibular Neuronitis: hours to days
BPPV: seconds to minutes
Menieres: minutes to hours
When do people with BPPV have symptoms?
patients are often
symptomatic when rolling over in bed
or moving their head to a position of
extreme posterior extension (such as looking up at a tall building or getting their hair washed at the hairdresser)
Patho of BPPV
due to canalithiasis (migration of free foating otoliths within the endolymph of the semicircular
canal) or cupulolithiasis (otolith attached to the cupula of the semicircular canal)
Causes of BPPV
head injury, viral infection (URTI), degenerative disease, idiopathic
Basic patho of meniere’s
inadequate absorption of endolymph leads to endolymphatic hydrops (over accumulation) that
distorts the membranous labyrinth
What age is most affected my Meniere’s?
Usually unilateral or bilateral?
peak incidence 40-60 yr
bilateral in 35% of cases
Clinical features of Meniere’s
- episodic vertigo, fuctuating low frequency SNHL, tinnitus, and aural fullness, ± drop attacks
± N/V - attacks come in clusters and can be debilitating to the patient
T/F the hearing loss of Meniere’s disease is transient. Normal hearing is preserved after the episode.
False
vertigo disappears with time (min to h), but HL remains
* early in the disease: fluctuating SNHL
* later stages: persistent tinnitus and progressive HL
Triggers for Menieres episodes?
high salt intake, caffeine, stress, nicotine, and alcohol
Management of Meniere’s (short and longterm)
acute management may consist of bed rest, antiemetics, antivertiginous drugs (e.g. betahistine
(Serc®), meclizine, diphenhydramine), and anticholinergics (e.g. scopolamine)
- long-term management may include
■ medical
◆ low salt diet, diuretics (e.g. hydrochlorothiazide, triamterene, amiloride)
◆ Serc® prophylactically to decrease intensity of attacks
◆ intratympanic gentamicin to destroy vestibular end-organ, results in complete SNHL
◆ intratympanic glucocorticoids (e.g. dexamethasone) may improve vertigo symptoms
What is Vestibular Neuronitis (Labyrinthitis)?
Classic presentation?
- acute onset of disabling vertigo ofen accompanied by N/V and imbalance without HL that resolves
over days, leaving a residual imbalance that lasts days to weeks - vestibular neuronitis: infammation of the vestibular portion of CN VIII
- labyrinthitis: infammation of both vestibular and cochlear portions
Etiology of Vestibular Neuronitis (Labyrinthitis)
thought to be due to a viral infection (e.g. measles, mumps, herpes zoster) or post-viral syndrome
* only ~30% of cases have associated URTI symptoms
* labyrinthitis may occur as a complication of acute and chronic otitis media, bacterial meningitis,
cholesteatoma, and temporal bone fractures
S&S of Vestibular Neuronitis (Labyrinthitis)
Acute vs convalescent phase
How long does severe vertigo usually last?
- acute phase
SINGLE EPISODE, SUDDEN ONSET, LASTS DAYS
■ severe vertigo with N/V and imbalance lasting 1-5 d
■ irritative nystagmus (fast phase towards the ofending ear)
■ ataxia: patient tends to veer towards afected side
■ tinnitus and HL in labyrinthitis - convalescent phase
■ imbalance and motion sickness lasting d-wk
■ spontaneous nystagmus away from afected side
■ gradual vestibular adaptation requires wk-mo
Treatment of Vestibular Neuronitis (Labyrinthitis)
- acute phase
■ bed rest, antivertiginous drugs
■ corticosteroids (methylprednisolone) ± antivirals
■ bacterial infection: treat with IV antibiotics, drainage of middle ear, ± mastoidectomy - convalescent phase
■ progressive ambulation, especially in the elderly
■ vestibular exercises: involve eye and head movements, sitting, standing, and walking
________ is the most common
intracranial tumour causing SNHL and
the most common CPA tumour
Acoustic neuroma
CPA = Cerebellopontine angle
Your elderly patient presents with unilateral tinnitus. You know that a good practitioner assumes the cause is ______ until proven otherwise
In the elderly, unilateral tinnitus or
SNHL is acoustic neuroma until proven
otherwise
What is an acoustic neuroma?
- schwannoma of the vestibular portion of CN VIII
tumour starts in the internal auditory canal and expands into CPA, compressing cerebellum and
brainstem
AKA Vestibular Schwannoma
Typical presentation of acoustic neuroma?
Is dizziness /vertigo common?
usually presents with unilateral SNHL (chronic) or tinnitus
* dizziness and unsteadiness may be present, but true vertigo is rare as tumour growth occurs slowly,
allowing for compensation to occur
* facial nerve palsy and trigeminal (V1) sensory defcit (corneal refex) are late complications
Gold standard diagnostic tests for acoustic neuroma?
MRI
How do we treat an acoustic neuroma in an elderly?
What is the definitive tx?
expectant management if tumour is very small or in elderly
- defnitive management is surgical excision
- other options: gamma knife, radiation
What is the HINTS examination?
The HINTS exam is a cluster of three bedside clinical tests that aim to assess individuals presenting with acute-onset dizziness, vertigo, nystagmus, head motion intolerance, and nausea/vomiting, also known as acute vestibular syndrome (AVS). HINTS is an acronym for the three tests included:
The Head Impulse Test (HI-)
Characterization of Spontaneous Nystagmus (-N-)
Test of Skew (-TS)
What is the Head Impulse Test (the HI in HINTS)
- Hold the patient’s head with both hands on either side and tilt the head slightly downward
- Encourage the patient to let their head relax in your hands to allow you to move back and forth and direct them to keep their eyes on your nose at all times
- Quickly move the head a small amplitude from central to the left of the right and back to the center again
- Try to randomly test left and right directions, as to not let the patient predict the movement
- Look for the patient’s loss of visual focus on your nose and a corrective saccade
Is an abnormal Head Impulse test indicative of peripheral or central causes of vertigo?
Peripheral
*the vestibulo-occular reflex is not preserved. Head movement causes eyes to move off target. Thsi is followed by a quick saccade (rapid jerky eye movement) back to target. The abnormal finding will occur with a head turn in only 1 direction.
How do you test nystagmus and how will it differ in central vs peripheral causes?
Have patient look left and right.
In central: will see direction-changing nystagmus, which will occur in the direction the patient is looking.
Peripheral: direction of the nystagmus remains the same when the patient looks left or right
What is the Test of Skew?
The patient is asked to look at the examiner’s nose. The examiners covers the left eye, then quickly moves the cover to the right eye. The left eye is observed for vertical (or diagonal) movement. The cover is moved back to the left eye. The right eye is assessed for vertical (or diagonal) movement.
How does the Test of Skew differ in patients with central vs peripheral causes?
Central: eye exhibits vertical or diagonal movement when cover is moved
Peripheral: skew is absent (normal test)
If you have focal neurologic findings or your HINTS exam shows any result consistent with central cause, what do you do?
Urgent neuroimaging
What is the most common central cause of acute-onset sustained vertigo?
Brainstem/cerebellar stroke
To recap, what findings on the HINTS exam most likely indicates a peripheral cause?
Abnormal Head Impulse test
Unidirectional nystagmus
Absent skew
(and no focal neurologic findings)
Thyroid labs:
Low TSH
Normal T4
Subclinical hyperthyroidism
Thyroid labs:
High TSH
Normal T4
Subclinical hypothyroidism
Thyroid labs:
Low TSH
High T4
Hyperthyroidism
When would you provide treatment for subclinical hypothyroidism?
TSH > 6.9, age less than 65-70, symptomatic
TSH 7-9.9, age less than 65-70
TSH 7-9.9, age greater than 65-70, symptomatic
TSH 10 or greater
Levothyroxine is the first line treatment for hypothyroidism. What is the typical target dose for a full replacement dose?
1.6 mcg/kg
How would your approach to initiating levothyroxine differ between a young healthy patient and an older adult (+/- coronary heart disease)
Young healthy people can be initiated at the full anticipated replacement dose (1.6 mcg/kg/day – 112 mcg for 70kg person)
Older adults, especially with cardiac history, should be started at a lower dose - between 25 and 50 mcg daily
What are the goals of hypothyroidism treatment?
relief of symptoms, normalization of TSH, reduction of goiter, avoidance of overtreatment
T/F: The target range for normal TSH differs in the older adult patient
True
Target range in younger people typically 0.5-5 mU/L
In older adults, upper limit of normal 7.5 mU/L
What would you expect to see for TSH/T4 with central hypothyroidism (abnormal hypothalamic-pituitary function)?
normal or low TSH
low or low-normal T4
What would you expect to see for TSH/T4 with hyperthyroidism due to abnormal hypothalamic-pituitary function?
TSH normal or high
T4 high
